
Class. 
Book 



COPYRIGHT DEPOSIT 



GENERAL AND DENTAL PATHOLOGY 



GENERAL AND DENTAL 

PATHOLOGY 

With Special Reference to Etiology and Pathologic Anatomy 
A Treatise for Students and Practitioners 



BY 

JULIO EXDELMAX, M.S., D.D.S. 

Professor of Special Dental Pathology, College of Dentistry, University of Southern 
California; Editor of the Pacific Dental Gazette; Member of the Southern Cali- 
fornia Dental Association, the California State Dental Association, and the 
National Dental Association; Corresponding Member of the Societe 
Odontologique de Fiance. Honorary Member of the Sociedad 
Odontologica de Chile, S. A., etc. 

AXD 

A. F. AYAGXER, A.M., M.D. 

Professor of General Pathology, College of Dentistry, University of Southern California; 
Pathologist and Autopsy Surgeon of the County and City of Los Angeles; Mem- 
ber of Dos Angeles County Medical Society, California State Medical 
Association, American Medical Association, etc. 



WITH 440 ILLVSTBATIONS, OF WHICH 340 IX THE SECTION ON 

DENTAL PATHOLOGY ABE ORIGINAL, AND 

FOUB CO LOP ED PLATES 



ST. LOUIS 

THE C. V. MOSBY CO. 
1920 






Copyright, 1920, By C. V. Mosby Company 

(All rights reserved) 



APR -8-1^0 



Press of 

C. V. Mosby Company 

St. Louis 



A56G420 



TO 

EDWARD C. KIRK, D.D.S., Sc.D., LL.D. 

Scientist, Teacher, Author 

From Whom the Authors Received the Instruction in 
Dental Pathology Which Constitutes the Foundation 
op the Section of This Book Devoted to That Purpose, 
and in Appreciation of His Contributions to Dental 
Science, This Book is Gratefully Dedicated. 



PREFACE 

It has been the aim of the authors to treat the subject from the 
standpoint of gross and microscopic pathology, realizing that the 
needs of the dental student call for just that character of infor- 
mation. It is, of course, assumed that the object in undertaking 
the study of pathology is to the effect that the information neces- 
sary to treat diseases upon a rational basis may be a Available ; there- 
fore the clinical aspects of the maladies discussed throughout the 
text have been worked out on the basis of the structural changes in- 
duced in the tissues by various forms of irritation. The clinic and 
the laboratory have been made use of extensively in the collection 
of the data and in their arrangement in sequential order, and an 
effort has been made to include only tangible information, excluding 
all statements of more or less speculative character. The book, it 
is hoped, will be a help to dental students by imparting a founda- 
tional knowledge of the subject and by rendering less complicated 
the interpretation of pathologic phenomena in the held of dental 
diagnosis. The comprehension of dental pathology rests upon a 
clear conception of those abnormal phenomena which, because they 
may develop in any organ or tissue of the body, are grouped under 
the heading of general pathology. Practically all the illustrations 
in the section on Dental Pathology are original, and this feature of 
the book, we trust, will greatly assist the student in his analysis of 
the pathologic anatomy of the diseases with which he concerns 
himself. 

AVe are greatly indebted to Dr. Lewis E. Ford for placing at our 
disposal the laboratories and clinical material of the College of 
Dentistry of the University of Southern California and for his 
friendly encouragement and help. To Dr. A. C. LaTouche we are 
indebted for many courtesies extended to us during the prepara- 
tion of the manuscript and illustrations and for the use of the 
microscopical sections from which Figs. 292, 293, and 405 were 
made, and for the original photograph of Fig. 401. 

To Dr. Carroll W. Jones, who greatly aided us in the preparation 
of the manuscript for the press and in the revision of the proofs, 
we gratefully acknowledge our appreciation. To Dr. James D. 



PREFACE 

McCoy the authors' thanks are due for repeated courtesies and sug- 
gestions and for his cooperation in gathering the data for the chap- 
ter on systemic infections ; all the radiographs in that chapter were 
supplied by Dr. McCoy, without whose assistance its preparation 
would have been greatly handicapped. To Dr. E. F. Tholen we ex- 
press our thanks for the originals of Figs. 346, 347, 348, and 349, 
and to Dr. C. F. Oakman for the use of Fig. 342. Our thanks are 
also due to Professor Wm. J. Gies, of Columbia University, for hav- 
ing placed at our disposal the literature covering his valuable inves- 
tigation in the domain of dental science ; from this we have quoted 
freely, especially in the chapter on dental caries. We are also in- 
debted to Dr. H. P. Pickerill for the use of Figs. 93, 94, and 95 
from his excellent work ' ' The Prevention of Dental Caries and Oral 
Sepsis. ' ' Our thanks for the loan of cuts are due to the publishers 
of the following works: Stengel and Fox's "Pathology," Bailey's 
"Textbook of Normal Histology," Delafield and Prudden's "Text- 
book of Pathology," McFarland's "Pathology," McConnell's 
"Pathology and Bacteriology for Dentists," Black's "Operative 
Dentistry," Ziegler's "Textbook of General Pathology," Blair's 
' ' Surgery and Diseases of the Mouth and Jaws, " " American Text- 
book of Dentistry, ' ' The Dental Cosmos, The Dental Summary, and 
others. The courtesy extended by Dr. F. "W. Frahm in offering sug- 
gestions which are incorporated in the chapter on macroscopic 
deformities is also acknowledged. The authors desire to thank 
Dr. W. A. Danielson of the Chicago College of Dental Surgery, 
for valuable suggestions in the text. 

To Dr. Gordon B. New of the Mayo Clinic, for contributing the 
chapter on Cystic Odontomas, and to Dr. J. Walter Reeves, for 
contributing the chapter on Malformations, the authors acknowl- 
edge their obligation. 

The authors wish to extend their thanks to the publishers for 
their hearty cooperation. 

Julio Endelman 
A. F. Wagner 

Los Angeles, Cal. 



CONTENTS 



PART I 
GENEKAL PATHOLOGY 

CHAPTER I 

PAGE 

Introductory 21 

Pathology, 21; Disease, 21; The Cell, 23; Anatomy of the Cell, 24; 
The Chemistry of the Cell, 26; The Physics of the Cell, 29; Stain- 
ing Reactions of the Cell, 30; The Physiology of the Cell, 32; Ori- 
gin of the Blastodermic Layers, "4. 

CHAPTER II 

The Etiology of Diseases 37 

Etiology of Disease, 37; Age, 28; Sex, 28; Race, 29; Idiosyncrasy, 
39; Traumatisms, 39; Injurious Occupations, 39; Unsanitary Sur- 
roundings, 40; Habits, 40; Heredity, 4; Specific or Determining 
Causes, 41; Traumatism, 41; Heat, 41; Cold, 42; Atmospheric Pres- 
sure, 43; Electricity, 43; Light, 4;'.; X-rays, 44; Chemical Agents, 
44; Living Organisms, 44; Autointoxication, 44. 

CHAPTER III 

Pathologic Processes 45 

Retrograde Processes, 45; Atrophy, 45; Degenerations (or Meta- 
morphoses), 47; Cloudy Swelling, Parenchymatous or Granular De- 
generation, 48 ; Patty Degeneration, 48 ; Mucoid Degeneration, 50 ; 
Colloid Degeneration, 52; Hyaline Degeneration, 54; Amyloid De- 
generation (Waxy, Bacony, or Lardaceous Degeneration), 56; In- 
filtrations, 59; Fatty Infiltration, 59; Pigmentary Infiltration, 61; 
Calcareous Infiltration, 67 ; Concretions of Concrements, 69 ; Hy- 
dropic, Dropsical, or Serous Infiltration, 70; Glycogenic or Glycog- 
enous Infiltration, 71 ; Necrosis, 72 ; Coagulation Neorosis, 73 ; 
Liquefaction Necrosis, 75; Cheesy Necrosis, or Caseation, 76; Fat 
Necrosis, 77; Focal Necrosis, 78; Gangrene, 79. 

CHAPTER IV 

The Circulatory Changes 82 

Ischemia, or Local Anemia, 82; Hyperemia, 83; Active Hyperemia, 



2 CONTENTS 

PAGE 
83; Passive Hyperemia, 84; Hypostatic Congestion, 85; Hemorrhage, 
85; Hemophilia, 87; Thrombosis, 87; Embolism, 90; Infarcts, 92; 
Edema, Dropsy or Anasarca, 95. 

CHAPTER V 

Inflammation 98 

Etiology, 98; Gross Pathology of Acute Inflammation, 98; Edema- 
tous or Serous, 100; Fibrinous, 100; Diphtheritic or Croupous, 100; 
Suppurative, 101; Abscess Formation, 102; Phlegmonous Inflamma- 
tion, 103; Catarrhal Inflammation, 104; Parenchymatous Inflamma- 
tion, 105; Interstitial Inflammation, 106; Hemorrhagic Inflamma- 
tion, 106; Necrotic or Gangrenous Inflammation, 106; Productive 
Inflammation, 106; Regeneration, 108; Pathologic Anatomy, 108; 
Pathologic Regeneration, 108; Metaplasia, 110; Heteroplasia, 110. 

CHAPTER VI 

Progressive Tissue Changes Ill 

Hypertrophy, 111; Etiology, 111; Gross Pathology, 112; Micro- 
scopic Pathology, 112; Pathologic Physiology, 112; Results, 112. 

CHAPTER VII 

Tumors 113 

Theories of Origin and Causation, 113; Fibromata, 117; Myxomata, 
119; Chondromata, 120; Chordomata, 121; Osteomata, 121; Odon- 
tomata, 122; Lipomata, 122; Sarcomata, 123; Round-celled Sar- 
comata, 124; Spindle-celled Sarcomata, 127; Melanotic Sarcoma, or 
Melanomata, 127 ; Giant-celled Sarcomata, 128 ; Rhabdomyomata, 130 ; 
Leiomyomata, 130 ; Glioma, 132 ; Glioma Ganglionare, or Ganglionic 
Glioma, or Neuroma, 133; Angiomata, 133; Papillomata, 135; 
Adenomata, 138; Carcinomata, 139; Epithelioma, 141; Adenocarcin- 
omata, 143 ; Scirrhous Carcinoma, 143 ; Medullary Carcinoma, 145 ; 
Endotheliomata, 146; Teratomata, 148; Dermoid Cysts. 148; Hyper- 
nephroma, 148; Cysts, 149. 

CHAPTER VIII 

The Pathology of Infectious Diseases 152 

The Pathology of Infectious Diseases, 152; Suppurative Diseases, 
154; Epidemic Cerebrospinal Meningitis, 156; Gonorrhea, 157; Soft 
Chancre, or Chancroid, 158 ; Pneumonia, or Pneumonitis, 159 ; Bron- 
chof>neumonia or Lobular Pneumonia, 161; Tuberculosis, 164; Lep- 
rosy, 167; Syphilis, or Lues (or "Gieat Pox"), 168; Glanders, or 
Equinia, 171; The Toxemic Diseases, 172; Tetanus or Lock Jaw, 



COXTENTS 5 

PAGE 

172; Diphtheria, 173; Asiatic Cholera, 173; Typhoid Fever, 171; 
Bacillary Dysentery, 175; Malta Fever or Mediterranean Fever, 176; 
Anthrax, 176; Malignant Edema, 177; Gaseous Edema, 177; Bu- 
bonic Plague, 176; Influenza, 178; Epidemic Conjunctivitis, 179; 
Whooping Cough or Pertussis, 179; Vincent's Angina, 179; Relaps- 
ing Fever, 179; The Higher Bacteria, 180; (Trichomycetes, Chalam- 
ydobacteriacese) , 180; Leptothrix Infections (Leptotrichoses), 180; 
Cladothrix and Xocardia Infections or Mycoses, 180 ; Actinomycosis, 
181 ; Mycetoma, or Madura Foot of India, 182 ; Blastomycosis or 
Saccharomycosis, 182 ; Oidiomycosis, 183 ; Mycoses due to Molds, or 
Hyphomycetes, 183; The Protozoan Infections, 185; Amebic Dysen- 
tery, 185; Trypanosomiasis, 186; Leishmaniases, 187; Malaria, 
187; Coccidiosis, 190; Infectious Diseases Caused by Undetermined 
Microorganisms, 190; Measles, 190; German Measles, 191; Chicken 
Pox or Varicella, 191; Scarlet Fever or Scarlatine, 191; Mumps, or 
Acute Epidemic Parotitis, 191 ; Acute Poliomyelitis, or Infantile 
Paralysis, 192 ; Acute Articular Rheumatism, 192 ; Dengue, 193 ; 
Yellow Fever, or Typhus Icteroides, 193; Typhus Fever, 191; Small- 
pox, or Variola, 191; Foot-and-mouth Disease, 191; Rocky Mountain 
Fever, 195; Metazoa, 195; The Cestodes, or Tapeworms, 198. 

CHAPTER IX 

Malformations 208 

Malformations by Excess, 208; Malformations by Defect, 209; Hare- 
lip and Cleft Palate, 211. 



PART II 
DENTAL PATHOLOGY 

CHAPTER X 

Introduction 213 

Predisposing and Exciting Causes, 213; Lowered Vital Resistance, 
211; Exciting Causes, 211; Predisposing Causes of Dental Disease, 
215. 

CHAPTER XI 

Enamel, Dentin, and Cementum 217 

Normal Histologic Considerations, 217; Normal Enamel, 217; Dentin, 
228; Cementum, 233. 



4 CONTENTS 

CHAPTER XII 

PAGE 

Development of the Teeth 241 

Dentin, 246; Cementum and Peridental Membrane, 248. 

CHAPTER XIII 

Hypoplasia, Microscopic and Macroscopic 250 

Dental Hypoplasia, 251; Enamel, Dentin, and Cementum, 251. 

CHAPTER XIV 

Macroscopic Deformities of the Teeth 264 

Abnormalities of Form Affecting the Crowns and Roots of the Per- 
manent Teeth, 264; Geminated Teeth, 284. 

CHAPTER XV 

Abnormalities in the Number of Teeth 287 

Supernumerary Teeth, 287. 

CHAPTER XVI 

Abnormalities in the Number of Teeth 291 

Absence of Teeth, 291. 

CHAPTER XVII 

Hutchinson's Teeth and Other Syphilitic Stigmata 299 

Hutchinson's Teeth and Other Syphilitic Stigmata, 299. 

CHAPTER XVIII 

Dental Caries 306 

Historical Data, 306. 

CHAPTER XIX 

Dental Caries (Cont'd ) 311 

General Considerations, 311; Predisposing Causes, 317. 

CHAPTER XX 

Pathologic Processes in Dental Caries 322 

Pathologic Processes in Dental Caries, 322. 

CHAPTER XXI 

Caries of the Enamel 331 

Etiology and Pathologic Anatomy, 331. 



CONTENTS 5 

CHAPTEE XXII 

PAGE 

Caries of Dentin and Cementum 340 

Etiology and Pathologic Anatomy, 340 ; Transparent Zone or Zone of 
Tomes, 344; Pigmentation, 347; The Decay of Cementum, 349. 

CHAPTEE XXIII 

Hypercementosis 350 

General Considerations, 350; Etiology and Pathologic Anatomy, 352. 

CHAPTEE XXIV 

Abrasion and Erosion 356 

Etiology of Abrasion, 356; Pathologic Anatomy of Abrasion, 357; 
Etiology of Erosion, 359; Pathologic Anatomy of Erosion, 365. 

CHAPTEE XXV 

The Saliva 366 

Normal and Pathologic Considerations, 366; Color, 367; Odor, 368; 
Taste, 368; Constituents of the Saliva, 369; Mucin, 369; Ptyalin, 
370; Albumin, 371; The Sulphoeyanatcs, 371; Inorganic Constit- 
uents, 372; Beaction, 373. 

CHAPTEE XXVI 

The Gums and Gingivae 375 

Normal and Pathologic Considerations, 375; Gingiva 1 , 376; Normal 
and Pathologic Considerations, 376; Functions, 378. 

CHAPTEE XXVII 

Calcareous Deposits 381 

Etiology, 381; Lesions in the Investing Tissues Caused by Salivary 
Calculi, 387. 

CHAPTEE XXVIII 

Subgingival Deposits 390 

Etiology, 390; Lesions Produced by Subgingival Deposits: Chronic 
Gingivitis, 392; Pathologic Anatomy, 392. 

CHAPTEE XXIX 

Diseases of the Peridental Membrane 402 

Horizontal Fibers, 405; Oblique Fibers, 405; Apical Fibers, 406; 
Alveolar Crest, 406; Free Gingiva, 406; Transseptal Fibers, 406. 



6 CONTENTS 

CHAPTER XXX 

PAGE 

Nonseptic Pericementitis 408 

Nonseptic Pericementitis, 408. 

CHAPTER XXXI 

Septic Pericemental Inflammation and Acute and Chronic Dento- 

alveolar abscess . 412 

Prophylaxis of Pulp Involvements, 414; Etiology of Septic Apical 
Pericementitis, 415; Periapical Infection by the Hematogenic Route, 
421; Recovery from Periapical Infections, Acute and Chronic Proc- 
esses, 422. 

CHAPTER XXXII 

Acute Apical Dentoalveolar Abscess 424 

Etiology, 424; Clinical Symptoms, 425; Sinus Formation, 427. 

CHAPTER XXXIII 

Pathologic Anatomy of Acute Dentoalveolar Abscess 433 

Pathologic Anatomy of Acute Dentoalveolar Abscess, 433. 

CHAPTER XXXIV 

Chronic Dentoalveolar Abscess 436 

Etiology and Pathologic Anatomy, 436; Difference in the Pathology 
of Acute and Chronic Dentoalveolar Abscess, 443 ; Bacteria of Septic 
Pericementitis and Dentoalveolar Abscess, 452. 

CHAPTER XXXV 

Bone 455 

Normal and Pathologic Considerations, 455 ; Bone Involvement in 
Dentoalveolar Abscess, 457; Necrosis, Caries, and Rarefying Ostei- 
tis of the Alveoli and of the JaAvs — Necrosis of the Apical Areas of 
Roots, 462. 

CHAPTER XXXVI 

Periostitis of the Jaw 467 

Periostitis of the Jaw, 467. 

CHAPTER XXXVII 

Pyorrhea Alveolaris 471 

Historical Sketch, 471; General Considerations, 473; Pyorrhea Al- 
veolaris Caused by Salivary Calculi, 474; Pyorrhea Alveolaris Caused 
by Subgingival Deposits, 476; Pyorrhea Alveolaris of Systemic Ori- 
gin, 487. 



CONTENTS i 

CHAPTER XXXVIII 

PAGE 

Pyorrhea Alveolaris and Pericemental Abscess of Gouty Origin . 495 
Etiology and Pathologic Anatomy of Pyorrhea Alveolaris and Peri- 
cemental Abscess of Gouty Origin, 496. 

CHAPTER XXXIX 

The Dental Pulp and Its Diseases 500 

Histologic Constituents, 500; Fibers of Tomes, 505; Diseases of the 
Pulp, 505; General Predisposing Causes, 506; Local Predisposing 
Causes, 507; Exciting Causes: General, 508; Exciting Causes: 
Local, 509. 

CHAPTER XL 

Calcific Degenerations of the Pulp and of the Dextixal Tubuli . 510 
Secondary Dentin, 510; Pulp Nodules, 514. 

CHAPTER XLI 

Pulp Hyperemia 518 

General Considerations, 518; Etiology, 519. 

CHAPTEE XLII 

Gangrene of the Pulp — Putrescent Pulp 523 

General Considerations, 523; Pulpitis, 525; Nonseptic Pulpitis, 525; 
Septic Pulpitis, 526; Pathologic Anatomy, 528; Pulp Hypertrophy, 
530. . 

CHAPTER XLIII 

Cystic Odontomas. (By G. B. New, M.B., Mayo Clinic, Rochester, 

Minn.) 532 

Simple Cysts of Type A, 532; Simple Cysts of Type B, 534 ; Adaman- 
tinomas, 535; Pathologic Anatomy, 539. 

CHAPTER XLIV 

Mouth Infections in Their Relation to Systemic Disease .... 544 
Secondary Focal Infections, 562. 

CHAPTER XLV 

Diseases of the Gingivae, Gums and Oral Mucous Membrane . . . 565 
Simple Stomatitis (Stomatitis Simplex), 565; Catarrhal Stomatitis, 
566; Ulcerative Stomatitis, 567; Mercurial Stomatitis, 569; Aphthae 
—Canker Sores — and Aphthous Stomatitis, 570 ; Thrush, 571 ; Herpes 
Labialis, 572; Affections of the Tongue, 572; Ulcers of the Tongue, 
572; Leucoplakia of the Tongue, 573. 



ILLUSTRATIONS 

FIG. PAGE 

1. Diagram of a typical cell 24 

2. Diagrams of successive phases of mitosis 34 

2. Diagrams of successive phases of mitosis 35 

3. Brown atrophy of the heart muscle 46 

4. Albuminous degeneration — kidney 47 

5. Fatty degeneration — kidney 49 

6. Mucoid degeneration of fibrous tissue 51 

7. Colloid degeneration of the thyroid gland 53 

8. Hyaline degeneration of an ovarian capillary 54 

9. Amyloid infiltration of capillary vails in kidney glomerulus .... 56 

10. Fatty infiltration of the liver 60 

11. Anthracosis of the lung 65 

12. Calcareous infiltration of the vail of a small artery from the wall of 

a gumma of the liver 68 

13. Dropsical infiltration of the epithelial cells of a carcinoma of the 

breast 71 

14. Coagulation necrosis of the hepatic cells in a case of puerperal 

eclampsia 74 

15. Large tubercle of the lung, showing cheesy necrosis 77 

16. Focal necrosis in the liver in pneumonia 78 

17. Senile dry gangrene of the lower extremity, showing line of demar- 

cation 80 

18. Chronic passive congestion of the liver 84 

19. Old anemic infarct of spleen 94 

20. Acute Inflammation 100 

21. Inflammation of the mesentery 100 

22. Acute inflammation 100 

23. Pseudomembranous inflammation of the uvula 101 

24. Tuberculous ulceration of the intestine 104 

25. Acute bronchial catarrh 105 

26. Chronic interstitial nephritis 105 

27. Loops of blood-vessels in granulation tissue 107 

28. Formation of new blood-vessels as seen in the tail of a tadpole . . . 107 

29. Fibroblasts forming fibrous tissue 108 

30. Eegeneration of epithelium 109 

31. Hard fibroma 117 

32. Soft fibroma of the subcutaneous tissue 118 

33. Section of a myxosarcoma 119 

34. Chondroma of the thumb 120 

35. Osteoma of the lower jaw 122 

8 



ILLUSTRATIONS V 

FIG. PAGE 

36. Small round-celled sarcoma 125 

37. Large round-celled sarcoma 126 

38. Alveolar sarcoma 126 

39. Spindle-cell sarcoma of the mammary gland 127 

40. Large spindle-celled sarcoma . . . . ' . 128 

41. Melanosarcoma 129 

42. Giant cell sarcoma of the thigh 129 

43. Metastatic melanosarcoma of lung 130 

44. Submucous fibroid in the uterus 131 

45. Glioma of the brain 132 

46. Cavernous angioma of liver 134 

4 7. Papillomata of the vocal cords 137 

48. Papilloma of the scalp 137 

49. Adenoma of the mammary gland 138 

50. Squamous epithelioma 142 

51. Adenocarcinoma of the body of the uterus 144 

52. Scirrhous carcinoma of breast 145 

53. Medullary carcinoma of breast 146 

54. Endothelioma of the dura mater 147 

55. Finer structure of the adenomatous form of hypernephroma . . . 149 

56. Chorionepithclioma or syncytioma malignum 150 

57. Cyst of the parovarium 151 

58. Acute urethritis 158 

59. Acute lobar pneumonia 160 

60. Acute lobar pneumonia. Later stage 161 

61. Bronchopneumonia. Child 162 

G2. Miliary tubercles in the liver 165 

63. Miliary tubercle of the human form 165 

64. Nodular leprosy 168 

65. Gummatous meningo-eneephalitis 170 

66. Typhoid fever, showing necrosis of Peyer 's patches and intense con- 

gestion of the bowel 175 

67. Actinomycosis of the tongue 181 

68. Blastomycosis 182 

69. Invasion of a human hair by trichophyton 184 

70. Trypanosoma gambiense 186 

71. The common liver-fluke enlarged to show the anatomic characters . 197 

72. Head of Taenia solium 198 

73. Taenia eehinococcus, enlarged 200 

74. Ascaris lumbricoides 201 

75. Male Trichocephalus dispar or whipworm 202 

76. Cephalic extremity of uncinaria duodenalis 203 

77. Duodenum showing attached uncinaria 203 

78. Trichina spiralis with its connective-tissue covering 205 

79. Filaria embryo, alive in the blood 206 



10 ILLUSTRATIONS 

FIG. PAGE 

SO. Female acarus 207 

81. Head of fetus at end of fifth week 210 

82. Head of fetus in the seventh week 210 

83. Diagram of ordinary harelip 211 

84. Almost complete single harelip 211 

85. Diagram of median harelip 211 

86. Cleft of the hard and soft palate . . . 212 

S7. Complete double cleft in an infant 212 

88. Area of normal dentin and enamel 218 

89. Area of normal dentin and enamel from ground section of area near 

apex of incisor of man 219 

90. Contrast between normal enamel and decalcified enamel .... 220 

91. Dentoenamel junction 221 

92. Ground section, showing junction of enamel and cementum . . . 222 

93. Imbrication lines on lower incisor of sclerotic type 224 

- 94. Imbrication lines on lower incisor of malacotic type 224 

95. Calcarine fissures on the surface of a malacotic molar 225 

96. Decalcified longitudinal section showing butt type of enamel-cemen- 

tum junction 227 

97. Longitudinal section of upper cuspid showing the course and ar- 

rangement of the dentinal tubuli (Color Plate) . . . . . 228 

98. A field of dentinal tubules 229 

99. Transverse section of dentin 229 

100. Intei globular spaces of Czermack in the dentin 231 

101. Longitudinal ground section of tootli showing fields of dentin and 

enamel 232 

102. Transverse ground section at the apical region of a root .... 234 

103. Transverse ground section of tootli at the beginning of apical third 

Of root 235 

104. Thick area of cementum in the bifurcation of the roots of a molar . 230 

105. Longitudinal ground section showing hyaline cementum, etc. . . . 237 

106. Ground section, longitudinal, showing gingival third of root . . . 238 
1.07. Ground section, longitudinal, showing hyaline cementum devoid of 

lacunae and canaliculi 238 

108. Longitudinal ground section of cementum, showing lacunae in areas 

near dentin and fibers of pericemental membrane incased in the ce- 
mentum 239 

109. Longitudinal ground section in gingival third 239 

110. The cementum in the apical region of the roots of an upper first 

bicuspid 240 

111. First evidence of tooth development 242 

112. A slightly later stage than in the preceding illustration 243 

113. The four sets of cells of the enamel organ 244 

11 t. Same stage of development as seen in the preceding illustration . . 247 



ILLUSTRATIONS 11 

FIG. PAGE 

115. Calcification of the deciduous teeth 248 

316. Calcification of the permanent teeth 248 

117. Hypoplastic defects of the enamel 251 

118. Hypoplastic defect of the enamel 252 

119. Hypoplasia of the enamel producing an external macroscopic defect 

on the labial surface of an incisor 255 

120. Hypoplasia of the enamel in the approximal surface of an incisor . 256 

121. A case of enamel agenesia 257 

122. Decalcified section showing a multitude of interglobular spaces . . 257 

123. Hypoplasia of the enamel in the shape of a slight reddish brown 

discoloration 259 

'124. Hypoplasia of the enamel in the shape of intense reddish brown dis- 
coloration 259 

125. A case of brown stain affecting the enamel on the labial surfaces of 

the central and lateral incisors only 259 

126. A slight hypoplasia of the enamel on the labial surface of an upper 

cuspid 260 

127. Hypoplasia of the enamel on the labial surface of an upper cuspid 260 

128. Hypoplasia of the enamel on the labial surfaces of upper left and 

upper right lateral incisors, semilunar in shape 260 

129. Hypoplasia of the enamel in an upper left central incisor .... 260 

130. Hypoplasia of the enamel in an upper right lateral incisor .... 261 

131. Hypoplasia in the crown of a lower molar 261 

132. Hypoplasia of the crown of an upper molar 261 

133. Hypoplasia of the enamel in upper molars 261 

134. Hypoplasia of the enamel in lower molars 262 

135. Hypoplasia of the enamel in an upper cuspid 262 

136. Hypoplasia of the enamel in an upper central 262 

137. Overdeveloped cervico-lingual ridge in upper left lateral incisor . 265 

138. Hypoplasia of the cervico-lingual ridge of upper incisors .... 265 

139. Fissured cervico-lingual ridge in lateral incisor 265 

140. Photomicrograph of a central incisor with an over-developed cervico- 

lingual ridge simulating a cusp 266 

141. Severe hypoplasia of upper central incisor 267 

142. Severe form of hypoplasia in upper incisor 267 

143. Severe form of hypoplasia in upper incisor involving the crown and 

the root 267 

144. Hypoplasia of the root of an upper incisor 267 

145. Ground section of specimen shown in Fig. 144 268 

146. Hypoplasia of the incisal third of an upper incisor 269 

147. Peg-shaped upper lateral incisor 269 

148. An upper right lateral incisor mesial view with a labial defection of 

its root 269 

149. A prong-like process on the lingual surface of the lower lateral in- 

cisor 269 



12 ILLUSTRATIONS 

FIG. PAGE 

150. Lower lateral incisor with tAvo roots 270 

151. Severe hypoplasia of upper cuspid 270 

152. A marked case of enamel and dentin hypoplasia 270 

153. A series of upper cuspids with unusually short roots 271 

154. A series of upper cuspids with abnormally long roots 271 

355. Distal deflection of an upper right cuspid 272 

156. A marked deflection to the mesial in an upper right cuspid . . . 272 

157. Lower cuspids with two roots 272 

158. Radiogram of a lower right cuspid with two roots 273 

159. Supernumerary root in lower cuspid 273 

160. Marked hypoplasia of the crown of a lower cuspid 273 

161. Upper first bicuspid with three roots 273 

162. Upper right first bicuspid with three roots 273 

163. An upper second bicuspid with a bifurcated root 273 

164. An upper first bicuspid with marked deflection of the lingual root . 273 

165. Bifurcation of the roots of an upper second bicuspid 274 

166. An upper bicuspid with three roots 274 

167. An upper first bicuspid with an abnormally long root 274 

168. A hypoplastic upper bicuspid . . 274 

169. Pronounced deflection of the root of an upper bicuspid 274 

170. Upper left second bicuspid; disproportion between the size of the 

croAAui and that of the root 275 

171. An upper second bicuspid with a disproportionately small root . . 275 

172. A lower first bicuspid AAith tAvo roots 275 

173. LoAver second bicuspid AAith tAvo roots 275 

174. A lower first bicuspid AAuth a marked deflection of its roots . . . . 275 

175. Distal deflection of the root of the lower right first bicuspid . . . 275 

176. Disproportion between the size of the crowns and roots of lower sec- 

ond bicuspids 276 

177. Hooked root in loAver bicuspid 276. 

178. Disproportion between the erown and root of a lower right second 

bicuspid 276 

1.79. Disproportion betAA y een the size of the crown and that of the root and 

deflections of the root of lower first bicuspids 276 

180. Hypoplasia of the lingual cusp of a lower first bicuspid .... 277 

181. A hypoplastic loAver second bicuspid 277 

182. LoAver left second bicuspid with six cusps 277 

183. The roots of an upper molar united by bands of cementum ... 278 

184. An upper second molar with its three roots fused together by means 

of cementum 278 

185. Upper left third molar with badly deflected, fused, and hyperce- 

mentosed roots 278 

186. An upper first molar with hooked roots 278 

187. Deflection to buccal and distal roots of upper first molar .... 279 

188. A supernumerary root in upper molar 279 



ILLUSTRATIONS 13 

FIG. PAGE 

189. Lower right first molar with supernumerary root on the lingual 

aspect 280 

190. Supernumerary root on distobuecal aspect of a lower first molar . . 280 

191. A lower first molar with a supernumerary root between the mesial 

and distal roots on the lingual aspect , 280 

192. A lower first molar with three roots 280 

193. A lower first molar with three roots; supernumerary root on incisal 

aspect 280 

194. Four well-developed roots in lower left second molar .... 281 

195. A hypoplastic lower third molar 281 

196. Dwarfed upper third molar 282 

197. Dwarfed lower third molars 282 

198. Dwarfed upper third molar 282 

199. Hypoplastic upper third molars 283 

200. Marked deviation of the roots of an upper third molar .... 283 

201. Upper third molars with double deflection of the buccal roots and 

single deflection of the lingual roots 283 

202. Geminated deciduous incisors 285 

203. Geminated upper central and lateral incisors 285 

204. Geminated molar and bicuspid; possibly two bicuspids .... 285 

205. Geminated upper second and third molars 285 

206. Geminated upper second and third molars 286 

207. Geminated upper second and third molars 286 

208. Enamel pearl on upper left second molar located in the concavity on 

the lingual root which shows a tendency toward bifurcation . . 286 

209. Enamel pearl in upper right first molar 286 

210. A peg-shaped supernumerary tootli between the upper central incisors 287 

211. Two tuberculated supernumerary incisors in the same arch . . . 287 

212. A tuberculated supernumerary tooth between the incisors .... 288 

213. A peg-shaped supernumerary tooth located lingually to the upper in- 

cisors 288 

214. A supernumerary central in perfect alignment between normal in- 

cisors 288 

215. A supernumerary upper incisor fused to the normal central incisor 289 

216. Supernumerary molar between the upper second and third molars . 289 

217. A fourth molar in place 289 

218. Deciduous upper second molar retained until late in life .... 292 

219. A retained lower left second deciduous molar 292 

220. Absence of the upper right lateral incisor 293 

221. Noneruption of permanent lower first molar 293 

222. Noneruption of permanent cuspid 294 

223. Noneruption of permanent cuspid 294 

224. Impaction of lower third molar 295 

225. Impaction of third molar 295 



14 ILLUSTRATIONS 

FIG. PAGE 

226. Impaction of lower third molar 296 

227. Impaction of second bicuspid and second molar 296 

228. Impacted lower third molar 297 

229. Hutchinson's teeth. Sulciform erosions of incisors 300 

230. Hutchinson teeth. Cuspal erosions of canines and molars .... 300 

231. Hutchinson's teeth. Cuspal atrophy of canines and first molars . . 301 

232. Multiple sulciform erosions, general, and involving the bicuspids . 301 

233. Lingual aspects of preceding illustrations. Hutchinson's teeth . . 301 

234. Hutchinson teeth. Honeycomb erosions 302 

235. Hutchinson teeth. Microdontism 303 

236. Complete congenital absence of teeth in the upper arch 303 

237. Defective fissure in a molar 318 

238. Typical conical form of penetration of caries into the dentin . . . 326 

239. Microorganisms in the structure of the dentin 327 

240. Microorganisms in the structure of the dentin . 327 

241. Microorganisms in the structure of the dentin 329 

242. Microorganisms in the structure of the dentin 329 

243. Artificial decalcification of the enamel by one per cent hydrochloric 

acid simulating caries . 332 

244. Caries of enamel at the deepest portion of the cavity 333 

245. Caries of enamel in proximal surfaces 335 

246. Caries of enamel in a proximal surface in which caries has made con- 

siderable progress 336 

247. Caries of enamel in a pit 337 

248. Progress of enamel caries in a molar 338 

249. Progress of enamel caries in a molar 339 

250. Caries of dentin showing decalcification of the organic constituents 

and conversion into a soft cartilaginous mass 340 

251. Caries of dentin showing decalcification of the inorganic constit- 

uents and conversion into a soft cartilaginous mass 341 

252. Undermining caries; destruction of tooth substance from within . 342 

253. Undermining caries; destruction of tooth substance from within . 343 

254. Undermining caries of approximal surface ; undecayed enamel cusp 

about to break away 344 

255. Caries of dentin 345 

256. Transparent zone of Tomes in dentin 346 

257. Caries of enamel and dentin 348 

25! 



Caries of ccmentum on labial surface of abraded upper left central 



incisor 348 

259. Hypercemcntosis of lower first bicuspid and deflection of its root . 350 

260. Hypercemcntosis in upper right second molar 350 

261. Hypercemcntosis in upper bicuspid 351 

262. Hypercemcntosis of root of lower molar, the two roots are united by 

a band of ccmentum 351 

263. Hypercementosis involving the three roots of an upper molar . . . 351 



ILLUSTRATIONS 15 

FIG. PAGE 

264. Hypercementosis involving the apical area of the three roots of an 

upper molar 351 

265. Excessive hypercementosis in a lower molar 351 

266. Excessive hypercementosis in a molar which rendered its removal 

difficult and entailed the fracture of the surrounding alveolar 

process 351 

267. Hypercementosis involving the three roots of an upper left first molar 352 

268. Hypcrcementosis of the posterior root of the lower first molar . . 352 

269. Nodular form of hypercementosis 352 

270. Resorption of dentin and obliteration of the resorbe 1 area by ce- 

mentum 353 

271. Hypercementosis accompanied by dentin resorption and filling in of 

the rcsorbed area of dentin by cementum 351 

272. Abrasion — mechanical wearing away of the cusps of a lower molar 357 

273. A series of incisors which have suffered from slight abrasion . . 35S 
271. Abrasion of the ineisal edg -s of two upper central incisors; brown- 
ish discoloration of exposed dentin 358 

275. Photomicrograph of ground section of one of the abraded teeth . 359 

276. Upper right cuspid 360 

277. Upper cuspids which for many years have been the seat of abrasion 360 

278. Abrasion of lower third molar. Complete wasting away of the crown 361 

279. Abrasion of lower third molar. Complete wasting away of the crown 361 

280. Spiral-shaped abrasion in upper loft cuspid caused by an ill-fitting 

-Lisp 361 

281. A series of abraded lower cuspids ,">61 

282. Abrasion of upper right central incisor 362 

283. Abrasion of lingual surface of upper left cuspid 362 

284. Abrasion of the labial surface of the lower right first bicuspid . . 362 

285. Cup-shaped abrasion in lower molars 362 

286. Cup-shaped abrasion in lower first molar 36.", 

287. Cup-shaped abrasion in a lower molar 363 

288. Cup-shaped abrasion in lower molar 363 

289. Abrasion in a deciduous molar 363 

290. Action of acid calcium phosphate in conjunction with friction . . . 364 

291. Tubular calcification in the dentin . . . 364 

292. Normal gingiva of sheep 376 

293. Gingiva? of sheep 377 

291. Human gingiva 378 

295. Salivary calculi en the lingual surfaces of the roots of lower cuspids 383 

296. Voluminous salivary calculus with shelf-like formation .... 384 

297. Salivary calculus with shelf-like formation 384 

298. Salivary calculus in lower right incisor 384 

299. Salivary calculus which had attained considerable size and had caused 

exfoliation of the tooth 384 



16 ILLUSTRATIONS 

FIG. PAGE 

300. Salivary calculus in lower incisor which had caused the exfoliation 

of the tooth 385 

301. Salivary calculus covering all of the crown and most of the root of 

the tooth 385 

302. Salivary calculus which covered a large area of crown surface and all 

of one-half the root surface 385 

303. Salivary calculus on lower right cuspid involving approximately two- 

thirds of the root 385 

304. Salivary calculus on lingual aspect of the root of a lower central 

incisor 385 

305. Salivary calculus covering portion of the labial surface of lower 

right central incisor 385 

306. Salivary calculus entirely covering the buccal surface of the crown 

and half the length of the roots of an upper left first molar . . 386 

307. Voluminous salivary deposits upon buccal and part of the occlusal 

surfaces of an upper molar 386 

308. Large masses of salivary calculi removed from the teeth to which 

they were attached 387 

309. Large masses of salivary calculi 387 

310. An upper lateral incisor with its root covered with subgingival de- 

posits 390 

311. Subgingival deposits in upjoer right lateral incisor 390 

312. Subgingival deposits in upper right cuspid 390 

313. Subgingival deposits in upper right second molar 391 

314. Subgingival deposits in upper right second molar 391 

315. Eoots of a molar covered with subgingival deposits 391 

316. Subgingival deposits on the anterior and posterior roots of a lower 

molar 391 

317. Section of human gingiva 393 

318. Chronic inflammation of gingiva 394 

319. Chronic inflammation of the free gingiva 395 

320. Gingivitis, chronic, advanced stage, infection progressing toward 

peridental membrane 396 

321. Gingivitis, chronic, advanced stage, induced by subgingival deposits 397 

322. Progressive chronic gingivitis 398 

323. Chronic inflammation of gingiva 399 

324. Chronic inflammation in the gingiva which has spread to the periden- 

tal membrane 400 

325. Progressive chronic gingivitis 401 

326. Normal peridental membrane 403 

327. Normal peridental membrane in situ 404 

328. Normal peridental membrane and its relation to cementum and al- 

veolar process 405 

329. Chronic dentoalveolar abscess of an upper lateral incisor with a large 

area of rarefaction 416 



ILLUSTRATIONS 17 

FIG. PAGE 

330. Chronic dentoalveolar abscess 416 

331. Chronic dentoalveolar abscess in upper first and second left bicuspids 416 






32. Three chronic dentoalveolar abscesses 416 

333. Chronic dentoalveolar abscess 417 

334. Chronic dentoalveolar abscesses 417 

335. Chronic dentoalveolar abscess 418 

336. Chronic dentoalveolar abscess , 418 

, 337. Chronic dentoalveolar abscess (so-called dental granuloma) . . . 419 

538. Chronic dentoalveolar abscess in the bifurcation of the roots of the 

lower right first molar 420 

339. Chronic dentoalveolar abscess caused by the perforation of the disto- 

lingual aspect of an upper second bicuspid 420 

340. Chronic dentoalveolor abscess caused by a fragment of a broach 

broken in the root canal 420 

341. Intraalveolar root fracture of an upper right cuspid 420 

342. Eesult of poulticing the face in connection with acute dentoalveolar 

abscesses 428 

343. Submental fistula 430 

344. A chronic dentoalveolar abscess (dental granuloma) 437 

345. Chronic dentoalveolar abscess 437 

346. Dentigerous or root cyst 442 

347. Dentigerous or root cyst 442 

348. Dentigerous or root cyst 442 

349. Dentigerous or root cyst 442 

350. Chronic dentoalveolar abscess (so-called dental granuloma) . . . 44 4 

351. Section of a chronic dentoalveolar abscess 44.1 

352. Chronic dentoalveolar abscess 446 

353. Chronic dentoalveolar abscess 447 

354. Chronic dentoalveolar aliscess 448 

355. Chronic dentoalveolar abscess 449 

356. High power reproduction of cellular elements in the round-cell infil- 

tration in a chronic dentoalveolar abscess 450 

357. Alveolar bone in the periapical region 458 

S58. Transverse section of tooth 459 

359. Arrangement of cancellated bone in region of central incisors . . 460 

360. Bone of alveolar process and two cancellated spaces 460 

361. Arrangement of bone in incisal region 461 

362. Arrangement of bone in bicuspid region 461 

363. Arrangement of bone in molar region 461 

326. Beginning resorption of the apical third of a root of an upper central 465 

365. Eesorption of the roots of a lower right first molar 465 

366. Beginning resorption of the apical third of a root of an upper central 465 

367. A chronic alveolar abscess 465 

368. Chronic dentoalveolar abscess 466 



18 ILLUSTRATIONS 

FIG. PAGE 

369. Sequestrum that came away attached to a tooth following a chronic 

dentoalveolar abscess of long standing 468 

370. Subgingival deposits on the root surfaces 475 

,371. Absence of approximal contact accounting for the formation of a 

pocket between lateral incisor and cuspid 475 

'372. Absence of contact and pyorrhea pocket formation 475 

373. Absence of contact and pyorrhea pocket formation ...... 475 

374. Absence of contact and pyorrhea pocket formation 475 

375. Absence of contact and pyorrhea pocket formation 475 

376. An area of gingivae from a pyorrhea pocket, the seat of a chronic 

inflammation 476 

377. Gum tissue overlying a pyorrhea pocket decalcified section . . . 477 

378. Chronic gingivitis which by process of continuity will spread to the 

gums and peridental membrane 478 

379. Decalcified transverse section of upper incisor 479 

380. An area of peridental membrane the seat of chronic inflammation 

in pyorrhea alveolaris 480 

381. Chronic inflammation of peridental membrane 481 

382. Transverse section showing dentin, eementum, peridental membrane, 

etc 482 

383. An infection from the peridental membrane involving the medullary 

substance in the cancellated space, an osteomyelitis being the re- 
sult 483 

384. Destruction of alveolar process and peridental membrane .... 484 

385. Destruction of the alveolar process and peridental membrane in 

pyorrhea alveolaris 484 

386. Absorption of the apical areas of the roots of the upper central in- 

cisors caused by infection 484 

387. Radiograms showing error in technic of taking 485 

388. Destruction of the alveolar process and peridental membrane . . . 485 

389. Destruction of the alveolar process and peridental membrane . . 485 

390. Destruction of the alveolar process and peridental membrane in 

pyorrhea alveolaris 486 

391. Destruction of alveolar process and peridental membrane in pyorrhea 

alveolaris 486 

392. Destruction of alveolar process and peridental membrane in pyorrhea 

alveolaris 486 

393. Destruction of alveolar process and peridental membrane establishing 

a pocket distal to the first molar 486 

394. Extensive pockets involving all the roots of lower first and second 

molars , 486 

395. Extensive destruction of alveolar process in pyorrhea alveolaris . 486 

396. Pyorrhea alveolaris 187 

397. Pyorrhea alveolaris in the lower teeth 488 

398. Pyorrhea alveolaris in the upper right cuspid 488 



ILLUSTRATIONS 19 

FIG. PAGE 

399. Pyorrhea alveolaris 489 

400. A typical case of pyorrhea alveolaris 489 

401. Destruction of alveolar process in an extensive case of pyorrhea 

alveolaris 490 

402. A longitudinal section of a normal pulp of man 501 

403. Longitudinal section of normal pulp 502 

404:. Section of tooth showing relation of the pulp at the apical foramen 

to the peridental membrane 503 

405. Section of a pulp of sheep, showing histologic characteristics of 

odontoblastic layer (Color Plate) 504 

406. Secondary dentin 512 

407. Secondary dentin which entirely filled the pulp chamber .... 513 

408. Secondary dentin in connection with abraded upper central . . . 513 

409. Secondary dentin in connection with severe abrasion 513 

410. Pulp the seat of a chronic inflammation 513 

411. Chronic inflammation of the pulp 514 

412. Pulp stones occupying the entire pulp chamber 515 

413. Pulp stone (nodule) in pulp chamber of lower molar 515 

414. Pulp nodule filling up the- entire pulp chamber 515 

415. A pulp nodule in situ 515 

416. Decalcified section with pulp stone in situ 516 

417. Decalcified longitudinal section, showing pulp stone in place . . 516 

418. Pulp stones in situ (Color Plate) 516 

419. Pulp stones in situ (Color Plate) 516 

420. Pull - ) stones in pulp chamber of upper right first and second molars 517 

421. Section of dental pulp, Longitudinal 519 

422. Cross section of hyperemia pulp 520 

423. Longitudinal section of a dental pulp, the upper portion of which 

has besn the seat of suppuration 529 

424. Simple cyst 533 

4 25. Adamantinoma 536 

426. Roentgenogram showing entire absence of ramus of jaw on right side 

and tumor extending across midline to bicuspid region on left side 537 

427. Adamantinoma 539 

428. Adamantinoma 540 

429. Section of adamantinoma 541 

430. Section of adamantinoma. 541 

431. Section of adamantinoma 542 

4M2. Cystic cavities in adamantinoma 542 

4 33. Portion of a mandible with cortical layer of bone removed . . . 545 

434. Vertical gross section of mandible in molar region 546 

435. Decalcified transverse section of upper central incisors 546 

436. Radiograph of case of systemic involvement 555 

437. Radiograph of case of systemic involvement oo(5 

438. Radiograph of case of systemic involvement 557 



20 



ILLUSTRATIONS 



FIG. PAGE 

439. Eadiograpli of case of systemic involvement 558 

•440. Eadiograpli of case of systemic involvement 558 

441. Eadiograpli of ease of systemic involvement 559 

442. Eadiograpli of ease of systemic involvement 560 

443. Eadiograpli of case of systemic involvement 560 

444. Ulcerative stomatitis (Color Plate) 568 



GENERAL AND DENTAL PATHOLOGY 



PART I 
GENERAL PATHOLOGY 



CHAPTER I 
INTRODUCTORY 



Pathology is the science which treats of the causes, manifesta- 
tions, and results of disease. Broadly speaking, pathology stud- 
ies disease in all its phases, but the bulk of the clinical symp- 
toms and the treatment, which constitute so large a field of in- 
vestigation, are usually dealt with in other departments of medical 
science. 

Disease 1 is any alteration of the structure or the composition 
of the tissues, which impairs or tends to impair their function. 2 
Disease is not an established entity, but a process. It is a continu- 
ing series of alterations which go on until interrupted by death, 
or until recovery takes place. The examination of a pathologic 
specimen shows the changes in structure and composition which 
have taken place up to the time when the tissue was examined; 



1 It is often contended that disease can not be accurately or scientifically defined, that 
there is no clearly marked dividing line between health and disease. This is undoubtedly 
true, but the same objection obtains against a definition of insanity, abnormality, hys- 
teria, death and many other terms. Tint few terms could be defined, if an absolutely un- 
assailable and faultless definition were demanded. A definition that would include all path- 
ologic manifestations and exclude all normal variations is neither possible nor necessary. 
It is far more important that the general reader, and particularly the student who is just 
beginning the study of pathology, should learn the meaning of terms as they are generally 
used and understood by pathologists, than that our definition should be scientifically 
flawless. 

2 "Just as physiology is the study of the functions of the body in health, so is pathology 
the study of the same functions in disease." — Adami. 

"* * * disease is not a thing, but a process. It is an abnormal performance of cer- 
tain of the functions of the body." — Delafield jmd Prudden. 

"It is doubtful whether alterations of function can occur without some alteration in 
structure." — Stengel and Fox. 

21 



22 GENERAL PATHOLOGY 

later examinations will reveal further alterations, and in many 
instances additional pathologic processes. 

Health is that state or condition in which the tissues and organs 
of the body are enabled to perform all their functions in a normal 
manner. It is of course impossible, with any great degree of 
exactitude, to point out where normality ends and abnormality 
begins, so gradually does the one condition merge into the other. 
The nearer we approach the boundary line, the more difficult it 
becomes to determine whether we are face to face with a normal 
variation of health or incipient disease. This difficulty, how- 
ever, disappears when a well-marked instance of disease is met 
with, and the task then resolves itself into a determination of 
the nature and extent of the morbid process. 

Health then is the performance of all the functional activities 
of the body in a normal (i.e., an average, regularly established) 
manner, and disease is impairment of these activities. In those 
eases where function is pathologically increased, as in the hy- 
pertrophies, the increase is at most only temporary and tends 
toward impairment later; in fact, when considered as a part of 
the sum total of activities which must act in harmony to con- 
stitute a state of health, any pathologic increase of functional 
activity must be regarded as an impairment of health. 

Life and functional activity are one and the same thing. Let 
one of the vital organs cease to do its work and death ensues. 
So far as biological science can determine, life is the result of 
chemical (more correctly, physicochentical) processes occurring 
within the tissues. When these processes are so coordinated 
that all the organs perform their activities in perfect harmony 
with one another, the individual is said to be healthy; when these 
processes are stimulated or retarded, by any cause whatsoever, 
beyond the normal, disease results. These abnormal chemical 
changes in the tissues can often be demonstrated by means of 
staining and other reactions before structural changes manifest 
themselves, and in all cases precede the latter. Chemical and 
structural changes result in changes of function, that is, disease. 
The so-called "functional diseases" 3 as for example, epilepsy, are 
such as exhibit decided functional changes, without discoverable 



3 Green's Pathology, p. 



INTRODUCTORY 23 

anatomic or chemical changes, but these undoubtedly exist and 
have caused the functional disturbance. 

Pathology therefore studies the morbid side of anatomy, chemis- 
try, and physiology, and it follows that a comprehensive knowledge 
of normal anatomy, chemistry, and physiology is a prerequisite to 
the study of pathologic conditions. 

THE CELL 

The living organism, animal and vegetable, is made up wholly 
of cells. Although recognized much earlier, the cell was not gen- 
erally accepted as the structural unit until Virchow founded 
modern pathology by the publication of his epochal work on 
Cellular Pathology in 1858. Since then it has also become the 
basis of chemical and physiologic considerations, and the cell is 
now the histologic, the chemical and the physiologic or biological 
unit. 

All organisms, unicellular and multicellular, are derived from 
a parent cell ("omnis cellula e cellula" — Virchow). The uni- 
cellular organisms, as protozoa and bacteria, arc composed of 
but one cell, which is capable of performing all ihe essential vital 
functions. In the multicellular organisms, the cells, after a suffi- 
cient number have been formed from the parent cell, form groups 
which become differentiated during the course of the development 
of the embryo, and destined to perform differenl functions. Such 
differentiated or specialized groups of cells with their character- 
istic intercellular substance (the latter being in all instances a 
product of the cells themselves) constitute the various tissues; 
appropriate amounts and kinds of different tissues form organs; 
and a system of organs with their supporting structures form 
the individual organism. 

Protoplasm is a term given to the albuminous material which 
composes the cell and gives to it its vital properties. It is not 
synonymous with cytoplasm (q.v.) or any histologic division of 
the cell. It is the basic substance found in all parts of the cell. 
Structurally the cell may be divided into two essential parts — 
the cytoplasm and the nucleus. Given these two essentials, a 
cell can perform all its physiologic functions, and may there- 
fore be considered a true cell. In addition to these two parts, 
the vegetable cells and some of the animal cells have a peripheral 



24 GENERAL PATHOLOGY 

membrane, or cell wall; and some cells, particularly when in an 
actively reproducing state, contain a body called the centrosome. 
A typical cell, therefore, may be said to consist of the follow- 
ing structures: 

Anatomy of the Cell 

1. A cell wall, or membrane. 

2. Cytoplasm, or cell material exclusive of the nucleus. 

3. The nucleus, or karyon (literally, a nut or kernel). 

4. Centrosome, lying within its centrophere. 

The cell wall, or membrane is a condensation and modification 
of the peripheral cytoplasm, which governs the entrance and 




..«-" 


~- 8 


^ 


.— 9 


£V-; 


..10 


-:'t\ 




y \\ 




~-^:;\ 


--*"// 


y*-Ji 


12 






L^z 


13 


£«*-.. 


-74 



2 

5 
6 

r 



Fig. 1. — Diagram of a typical cell. (After Bailey.) /, Cell membrane; 2, metaplasm; 
3, karyosome; 4, hyaloplasm; 5, spongioplasm ; 6, linin; 7, nucleoplasm; 8, attraction 
sphere; 9, centrosome; 10, plastids; //, chromatin network; 12, nuclear membrane; 13; 
nucleolus; 14, vacuole. 

exit of nutritive substances excretory products and other ma- 
terials. Only a few of the animal cells, such as fat cells, goblet 
cells, cartilage cells, etc., have a distinct cell wall; the great 
majority of animal cells present merely a more or less homo- 
geneous outer layer of cytoplasm, called ectoplasm or exoplasm, 
to distinguish it from the inner endoplasm which is usually granu- 
lar, and the phenomena of diffusion and osmosis indicate that 
the ectoplasmic zone serves the purposes of a cell wall. 

Vegetable cells have distinct cell walls, which often contain 
cellulose or chitin. The former appears as a blue circle on the 
application of iodine. 



INTRODUCTORY 25 

The cytoplasm, or cell body, is a semifluid substance composed 
of a network of fibrils (cytoreticulum) called spongioplasm, in the 
meshes of which is found a clear, glass-like, homogeneous, semi- 
fluid substance called hyaloplasm (also paraplasm). 

The actual structure of the spongioplasm is still a mooted ques- 
tion. Altmann believed it to be made up of granules lying in a 
gelatinous substance. He believed these granules to be the vital 
elements of the cell and called them oioolasts. Butchli's "foam" 
theory considers the reticular appearance of the spongioplasm to 
be due to a foam-like emulsion produced by the mixture of fluid 
of different degrees of viscosity, the cut walls of the minute 
foam spaces resembling a network. Others still believe the 
spongioplasm to be a feltwork of independent fibrils (filar mass 
or mitome). 

Within the cytoplasm are often found granules of pigment or 
secretory products, fat globules, substances in vacuoles, etc., 
which are collectively called metaplasm or paraplasm (though 
some writers use the latter term as synonymous with hyaloplasm). 
These cell inclusions are adventitious bodies and not true con- 
stituents of the cell. 

Plastids or protoplasts are bodies often occurring in vegetable 
cells, less often in animal cells, which are usually regarded as 
local areas of cytoplasm, specialized for the performance of some 
function, e.g., the transformation of starch, etc. 

The nucleus is a vesicular body, which in general conforms to 
the shape of the cell, being elongated in muscle and connective 
tissue cells, flat in epithelial cells, etc. Its morphology, however, 
may be very irregular, as seen in leucocytes, and the large bone- 
marrow cells (megakaryocytes). The typical cell contains but one 
nucleus, while the osteoclasts and the various giant cells are mul- 
tinucleated, resulting probably from repeated division of the 
nucleus without corresponding division of the cytoplasm. 

The vegetative nucleus (one not in active process of division) 
has a transparent, faintly staining nuclear wall or membrane 
(amphipy renin). 

The substance of the nucleus, or karyoplasm structurally re- 
sembles the cytoplasm in being composed of a network of fibrils 
(nucleorct tail urn) and an interfibrillar semifluid material (nucleo- 
plasm, nuclear matrix). 



26 GENERAL PATHOLOGY 

The nucleoreticulum consists of an achromatic, faintly staining 
network of fibrils (or linin), which supports in its meshes a deeply 
staining substance, called chromatin because of its great affinity 
for basic dyes. At the nodal points of the linin, the accumula- 
tions of chromatin into conspicuous granules are called karyo- 
somes (or net knots or false nucleoli). As usually stained the 
nuclei of many cells appear to be composed almost solidly of 
chromatin, because the latter stains deeply, while the linin and 
nucleoplasm stain faintly. 

The nucleoplasm or matrix is a clear fluid or semifluid sub- 
stance, lying in the meshes of the nucleoreticulum, probably nu- 
trient in character, resembling the hyaloplasm of the cytoplasm. 

The nucleolus, or plasmosome, is a small spherical body, some- 
times more than one, lying within the nucleus. It does not ap- 
pear to be attached to the nuclear structures, stains less in- 
tensely than the chromatin, particularly in fixed tissues, where it 
elects the acid stains, resembling in this respect the cytoplasm. 
Its function is not known. 

Cells without nuclei, as the red blood cells, are no longer true 
or complete cells, having lost the nuclei which all such cells pos- 
sessed in their early life history, together with their power of 
reproduction. 

In some of the simple forms of life, as bacteria, the nucleus 
either fills the whole cell, leaving an almost undemonstrably 
small ring of cytoplasm about the nucleus; but according to the 
more generally accepted view, the nuclear material, instead of 
being collected together into a compact nuclear body, is scat- 
tered throughout the entire cell. Bacterial cells, therefore, re- 
semble the nuclei of tissue cells in staining solidly and in hav- 
ing the same affinity for basic dyes. 

The centrosome is a very minute body of variable staining 
quality, and often difficult to distinguish from metaplasmic gran- 
ules. It is usually found in the cytoplasm near the nucleus, and 
is often surrounded by a clear area, the centrosphere, from which 
radiations into the surrounding cytoplasm may be seen when the 
cell is about to divide. 

The Chemistry of the Cell 

Protoplasm, or bioplasm, is the soft, colorless, jelly-like sub- 
stance of which living cells or tissues are composed. There is 



INTRODUCTORY 27 

no way of chemically analyzing living protoplasm. Chemical 
reagents cause the death of the cells with coagulation of various 
constituents, etc., hence the term "protein" (given to the most 
important constituent of protoplasm) refers necessarily to what 
the chemist finds when he analyzes dead cells, while the term 
"proteinogen" may be applied to the living material. 

Thus analyzed, cells are found to be composed essentially of 
proteins, lipoids, inorganic salts and water, often called the primary 
constituents. Other substances as fats, carbohydrates, secretory 
granules, pigment granules, enzymes, etc., are food mate- 
rials and metabolic products, and are not essential chemical com- 
ponents of the cell. These are often called secondary constit- 
uents, and it is these secondary constituents that account for 
the great differences in the histologic appearances of the various 
types of cells. 

Proteins are the most complex substances known to the chemist. 
They will not diffuse through animal membranes or other dif- 
fusion membranes, and some fail even to pass through fine porce- 
lain filters, hence their molecules must be very large. Both their 
structural and molecular formulae are as yet unknown, and even 
their empiric or percentage formulae have only been approxi- 
mately determined. For example, the percentage composition 
of oxyhemoglobin (one of the simplest of the proteins) varies 
according to different analyses; perhaps the most trustworthy 
being C 658 H 1181 O 210 N 207 S 2 Fe ; while the molecular weight accord- 
ing to different reports varies from 15,000 to 17,000. 

By hydrolysis of the proteins, with acids, alkalies, steam or 
enzymes, they yield successively, although not wholly synchron- 
ously, proteoses, peptones and peptides (which still retain certain 
properties characteristic of proteins) and finally amino acids — 
the "building stones" or ultimate constituents of the protein 
molecule. These amino acids are optically active, crystalloid sub- 
stances, of known chemical structure. Each contains an acid 
(carboxyl) group and a basic (amin) group, and is therefore am- 
photeric in reaction. Their type formula is 

NH 2 O 

! " II 

E—CH— C— O— H 



28 GENERAL PATHOLOGY 

Eighteen of these acids have been identified; all contain the 
amino-acid radicle combined with other groups or "nuclei," and 
the latter may belong to the aliphatic, or open-chain series (as 
glycocoll), homocyclic (as tyrosin) or heterocyclic (as trypto- 
phane). 

All protein food materials are reduced by the digestive enzymes 
into amino acids, preparatory to assimilation by the cell; after 
their introduction into the cell, the amino acids are synthesized 
by the intracellular enzymes into such type of proteins as the 
cells may need. 

Proteins have been classified as follows: 4 

I. Simple Proteins. Substances which yield only amino acids 
on hydrolysis. 

(a) Albumins, as egg albumin, serum albumin, lactalbumin. 

(b) Globulins, as serum globulin, ovoglobulin (from yolk of 
egg). 

(c) Glutelins, as glutenin from wheat. 

(d) Prolamins, as hordein from barley. 

(e) Albuminoids or scleroproteins, as collagen, elastin and 
keratin, from fibrous tissues, elastic tissues and skin appendages 
respectively. 

(f) Histones, as globin from hemoglobin. 

(g) Protamins, the simplest natural proteins, as salmine. 

The simple proteins differ among themselves in solubility, 
coagulability and other properties. 

II. Conjugated or Compound Proteins. 

(a) Nucleoproteins. Compounds of protein molecules and nu- 
cleins. The nucleins yield on further hydrolysis other protein 
molecules and nucleic acids. Nucleic acids are rich in phosphorus, 
being composed of phosphoric acid, pyrimidin bases, purin bases 
("nuclein bases") and a carbohydrate. The different combina- 
tions of these various ingredients result in an enormous variety 
of nucleoproteins, which constitute the most important part of 
the cell, both of cytoplasm and nucleus. 

(b) Glycoproteins. Compounds of protein molecules and a car- 
bohydrate group (other than that present in the molecule of nu- 
cleic acid), as the mucin of secretory cells, and the mucoid of 
fibrous tissues. 



4 The American Physiological Society and The American Society of Biological Chem- 
ists. 



INTRODUCTORY 29 

(c) PJiosphoproteins. Compounds of protein and phosphorus- 
containing substances (other than nucleic acid or lecithin), as 
casein from milk. 

(d) Hemoglobins. Compounds of protein with hematin or simi- 
lar substance, as hemoglobin from blood. 

(e) Lecithoproteins. Compounds of protein with lecithins (see 
below). 

Lipoids are substances which resemble fats in certain physical 
properties but differ chemically; they dissolve in ordinary fat 
solvents. The chief lipoids (or "fat-like" bodies) are lecithin 
and cholesterin. 

Lecithin is a combination of certain fatty acid radicals with phos- 
phoric acid and cholin, and constitutes the greater part of the 
lipoids. Lecithin plays a very important part in cell metabolism. 

Cholesterin, or cholesterol, is an alcohol, related to the terpenes. 
It is chemically rather inert, and its role is probably a physical 
one. 

Inorganic Salts, particularly chlorides, carbonates, phosphates, 
and sulphates of the alkaline metals and the alkaline earths, 
ionize in the water of the cell, and their ions unite chemically 
with the protein groups (ion proteins). It is very probable that 
proteins and lipoids engage in those chemical reactions, which 
are essentially the basis of life, only as they form compounds 
with the ions of inorganic salts. 

Water in generous amount within the cell is necessary to carry 
out the vital chemical processes, because it is the medium in 
which dissociation of the molecules of the salts above mentioned 
may take place, and the ions which are constantly liberated and 
reunited during the life of the cell become the electrolytes, bear- 
ing the electrical charges or energies which represent the fun- 
damental vital processes. 

The Physics of the Cell 

The substances before mentioned as essential or primary 
chemical constituents of the cell, together with the secondary 
constituents, are present in different physical states; viz., as 
colloids and crystalloids which are in solution, or semisolution, in 
the water and in each other. 



30 GENERAL PATHOLOGY 

It should be borne in mind that a solution is a physical condi- 
tion — a homogeneous mixture of molecules, and that ionization is 
an additional process whereby the molecules which have undergone 
solution are to a greater or less degree dissociated into atoms or 
groups of atoms electrically charged. When acids, bases, and salts 
"dissolve" in water, there is solution plus ionization. A sus- 
pension or emulsion is a more or less homogeneous mixture of mi- 
nute masses of molecules in a fluid. 

Colloids are substances which do not pass through diffusion mem- 
branes or do so very slowly. They are usually amorphous, but 
hemoglobin, egg albumin and certain other proteins crystallize 
readily. Colloids include all forms of proteins, the carbohy- 
drates (except the sugars), tannic acid, etc., also various in- 
organic compounds and metals. The protein colloidal solution 
is either a true solution of protein molecules, whose size, though 
undetermined, must be very great; or, as is more generally be- 
lieved, it is a suspension of minute masses of protein molecules. 
The colloids within the cell are therefore believed to be in 
a state of suspension. The foodstuffs of the cells — proteins, car- 
bohydrates and fats — in colloid form are first reduced to the 
crystalloid form of amino acids, sugar and diffusible soaps and 
glycerin respectively, and when these enter the cell through the 
cell wall, which acts as a diffusion membrane, pervious to water, 
salts, and crystalloids, but impervious to colloids, they are syn- 
thesized into colloidal proteins, fats, and carbohydrates again 
by aid of the intracellular enzymes. 

Crystalloids are substances which diffuse readily through the 
usual diffusion membranes, and tend to form crystals under 
favorable conditions. The cellular crystalloids include inorganic 
salts, sugars, amino acids, urea, creatinine, etc. The inorganic 
crystalloids or salts form ions, which carry electric charges 
and are therefore electrolytes. The organic crystalloids do not 
ionize and are nonelcctrolytcs. As Mann had stated, the elec- 
trolytes put life into the proteins. The organic crystalloids are 
chiefly important as foods or metabolic products. 

Staining Reactions of the Cell 

The cell protoplasm consists largely of nucleoproteins. 

In the cytoplasm all the primary constituents already men- 



INTRODUCTORY 31 

tioned are present, as well as many of the secondary constituents, 
but the nucleoproteins predominate, and consist of nucleic acid 
well saturated with protein materials, thus permitting the reac- 
tion of the cytoplasm as a whole to be neutral or slightly alkaline, 
in which condition it naturally elects the acid stains. 

The nucleus is very largely composed of nucleoprotein, but the 
nucleic acid portion of the molecule is not so well saturated with 
protein as in the cytoplasm, and the nucleus as a whole is acid 
in reaction and elects the basic stains. Because the unsaturated 
nucleoprotein stains so readily and intensely, it is called chro- 
matin. When the nucleus is in the process of mitotic division, 
the nucleic acid portion of the chromatin (nucleoprotein) becomes 
still less saturated than when in the resting or vegetative state, 
hence stains more intensely. 

The linin, as well as the nucleolus, is composed of well-satu- 
rated nucleoproteins, and therefore resembles the cytoplasm in 
staining reactions. 

The staining reagents most commonly used are the anilin dyes, 
manufactured from coal tar, and are derivatives of benzene and 
its homologues. Some of these stains are acid, others basic in 
reaction, and require tl^e opposite reaction in the tissues in order 
to stain well. 

The tissue elements may be classified into: 

(a) Oxyphil! ic, acidophillic or eosinophilic, which comprise the 
cytoreticulum, centrosomes, attraction spheres, nuclear mem- 
branes, linin, nucleoli and certain cytoplasmic granules. The 
general normal reaction of these elements is slightly alkaline. 

The more important of the acid or cytoplasmic dyes are eosin, 
erythrosin and acid fuchsin. 

(b) Basophilic, which comprise the substances rich in nucleic 
acid as chromatin and certain cytoplasmic granules (other than 
those already mentioned). 

The more commonly used of the basic dyes are hematoxylin, 
methylene blue, gentian violet, thionin blue, Bismarck brown and 
basic fuchsin. 

(c) Some tissue elements have the power of combining with, 
or absorbing either acid or basic dyes, and are therefore called 
amphophilic. 



32 GENERAL PATHOLOGY 

(d) Other elements, again, are stained by the neutral salt dyes, 
as the eosinate of methylene blue (Komanowski) and the triple 
stain of Ehrlich. The fine granules of the polymorphonuclear 
leucocytes are neutrophillic. 

The Physiology of the Cell 

All true cells (or those which have nuclei) have the funda- 
mental properties of nutrition, growth, irritability, motility and 
reproduction. 

Nutrition. — The cell is able to receive food substances from with- 
out and transform them into living protoplasm (anabolism) ; also 
to break down old and worn protoplasm into waste products (ca- 
tabolism), and extrude these from the cell. The sum total of these 
anabolic and catabolic chemical processes is called metabolism. 

Growth, or increase in size of the cell, is a natural consequence 
of nutrition, and is due to greater activity on the part of the 
anabolic than of the catabolic processes. 

Irritability. — This is a definite response to external stimuli. 
The character of the response depends upon the nature of the 
protoplasm ; the muscle cell contracts, the glandular epithelium 
secretes, and the nerve cell conveys impulses. 

Motility is the power of executing spontaneous movements and 
is exhibited in different forms : 

(a) Protoplasmic movement, which is an intracellular move- 
ment as shown by the circulation or " streaming " of the pro- 
toplasm. The minute granules, the nucleus, and other constit- 
uents move about, though in a restricted manner within the 
living cell. 

(b) Ameboid movement is a similar but more specific move- 
ment on the part of the protoplasm, consisting of a protrusion of 
certain parts of the cell (pseudopodia) beyond its usual outline. 
These pseudopodia may retract or may proceed until the whole 
cell has been drawn after them, changing both the shape and 
the position of the cell. 

(c) Ciliary movement is the wave-like motion of minute hair- 
like extensions of specialized cytoplasm, called cilia. Only the 
columnar variety of epithelium is ciliated. A cell may have 
from one to two dozen cilia. 



IXTRODUCTORY 33 

In all cases of cellular motion resulting in a change of shape of 
the cell, as in ameboid and ciliary motion, and in functionating 
muscle cells, it is the spongioplasm which contracts; the hy- 
aloplasm plays only a passive role and is believed to represent 
nutritive material. 

Reproduction is the derivation of one or more cells from a 
parent cell. Cell reproduction occurs in one of two ways — by 
direct cell division and by indirect division. 

In the direct form, amitosis, the nucleus divides without any 
demonstrable preliminary changes in its histology. This method 
of division is common in protozoa and other lower forms of life. 

In the indirect cell division, mitosis or karyokinesis, the nucleus 
passes through certain complex changes, and these changes, to- 
gether with alterations of other constituents of the cell, are usu- 
ally described as taking place in the following stages or phases: 

The Prophase, in which changes preparatory to division occur. 

The chromatin network is formed into one or more threads 
(skein or spireme), which later divides into segments (chromo- 
somes), the number of which is fixed and definite for each species 
of plant or animal cell. 

The centrosome develops a distinct attraction sphere and di- 
vides into two " stars" or asters, which separate, going to oppo- 
site poles of the cell, but still connected by fibrils of linin 
(achromatic spindle). The chromatin segments arrange them- 
selves along the equatorial line of the spindle. 

The nuclear membrane and nucleolus disappear during this 
phase. 

The Metaphase, in which actual division of the nucleus occurs. 

Each chromosome (or segment of chromatin) splits longi- 
tudinally, forming daughter chromosomes. 

The Anaphase, in which the changes are in the main the re- 
verse of those occurring in the prophase. 

The daughter chromosomes separate, one-half going to one pole 
along the linin threads of the achromatic spindle, the other half 
going to the opposite pole, where they form daughter nuclei. 

The Telophase, the finishing stage, in which the cell body di- 
vides at right angles to the axis of the spindle into two cells, each 
now having received an equal portion of the nucleus and one 



34 



GENERAL PATHOLOGY 



of the newly formed centrosomes. A nuclear membrane and a 
nucleolus appear in each new cell. Nothing is at present known 
regarding the function of the nucleolus. (Fig. 2.) 






Fig. 2. — Diagrams of successive phases of mitosis. 

A. Resting cell, with reticular nucleus and true nucleolus; c, attraction sphere with 
two centrosomes. 

B. Early prophase. Chromatin forming continuous thread — the spireme; nucleolus 
still present; a, ampliiaster; the two centrosomes connected by fibrils of achromatic 
spindle. 

C. Later prophase. Segmentation of spireme to form the chromosomes; achromatic 
spindle connecting centrosomes; polar rays; mantle fibers; fading of nuclear membrane. 

D. End of prophase. Monaster — mitotic figure complete; cp, chromosomes arranged 
around equator of nucleus; fibrils of achromatic spindle connecting centrosomes; mantle 
fibers passing from centrosomes to chromosomes. (E. 13. Wilson, "The Cell.") 



Origin of the Blastodermic Layers 

The matured ovum, after union with the spermatozoon has oc- 
curred (fertilization), enters upon a series of repeated divisions 
(segmentation). The first result is a solid spherical mass of cells 
(morula). This mass soon forms a cavity in its center, which 
grows until there is a hollow sphere (the blastodermic vesicle) sur- 
rounded by a single layer of cells attached to the inner surface 



INTRODUCTORY 



35 



of the vesicle except at one point of the inner surface where a 
small mass of cells persists which is called the embryonic area, 
because it is in this small mass of cells that the future enibrvo 







G H 

Fig. 2. — Diagrams of successive phases of mitosis. 

E, Mctaphasc. Longitudinal cleavage; splitting of chromosomes to form daughter 
chromosomes, ep; n, cast-off nucleolus. 

F, Anaphase. Daughter chromosomes passing along fibrils of achromatic spindle toward 
centrosomes; division of centrosomes; if, interzonal fibers or central spindle. 

G, Late anaphase. Formation of diaster; beginning division of cell body. 

H. Telophase. Reappearance of nuclear membrane and nucleolus; two complete 
daughter cells, each containing a resting nucleus. (E. B. Wilson, "The Cell.") 



first makes its appearance. As cell division proceeds, two layers 
of cells are produced; viz., the ectoderm, which corresponds to the 
original layer of the blastodermic vesicle, and the entoderm, or 
inner layer. Later a third layer appears between the ectoderm 
and the entoderm, called the mesoderm. The three layers together 
are called the blastoderm. 

The tissues derived from these layers are as follows : 

Ectoderm. — Epithelium of the skin and all its appendages, as hair, nails 
enamel of teeth, mammary, sebaceous and sweat glands, includ- 
ing the muscle of latter. 



36 GENERAL PATHOLOGY 

All epithelium not mentioned under mesoderm and entoderm, viz., 
the epithelium of mouth and nose with their glands and cavi- 
ties ; of membranous labyrinth of ear ; of anus and of that 
portion of male urethra anterior to the prostate gland. 

Entire nervous system, with the retina, crystalline lens, and mus- 
cle of the iris. 

Mesoderm. — All connective tissue. 

All muscle tissue, except as stated under ectoderm. 
All lymphatic tissue, spleen, hone-marrow and blood cells. 
All endothelium^- (of vessels and serous cavities). 
The epithelium of the genito-urinary tract, except ureter, bladder, 
female urethra and prostatic portion of male urethra. 

Entoderm. — Epithelium of alimentary tract (except mouth and anus) ; of 
Eustachian tube and tympanum. 
Epithelium of respiratory tract (except nose) ; also of thymus 
and thyroid glands. 

Epithelium of ureter, bladder, female urethra and prostatic portion 
of male urethra. 



1 The endothelia are included among the epithelia by some histologists; others again 
distinguish between the "endothelium"' of blood and lymph vessels, and the "mesothelium" 
ot serous cavities, the genito-urinary epithelium of mesodermal origin, and striated and 
heart muscle. 



CHAPTER II 

THE ETIOLOGY OF DISEASES 

While therapeutics is the art of healing disease, pathology is 
the science of investigating disease, and this investigation is 
usually pursued under the following headings : 

1. Etiolog}', or investigation of the causes of disease. 

2. Morbid, or pathologic anatomy, the changes of structure. 

3. Morbid, or pathologic chemistry, the changes in composi- 
tion. 

4. Morbid, or pathologic physiology, the changes in function. 
Of these, morbid anatomy lias been the most highly developed, 

and forms the major portion of the text in most works on pa- 
thology. 

Morbid anatomy, or morphologic pathology, is divided into : 

(a) Gross, or macroscopic pathology, dealing with the gross 
or naked-eye appearances, and 

(b) Pathologic histology, or microscopic pathology, dealing 
Avith minute or microscopic appearances. 

Etiology of Disease 

The causes of disease are usually divided into (a) predispos- 
ing, indirect or mediate causes, and (b) specific, direct, imme- 
diate, exciting or determining causes. Predisposing causes in- 
clude all conditions, influences and agencies which increase the 
individual's susceptibility to disease, while the specific causes 
are the direct and final factors which culminate in the outbreak 
of disease and determine its nature. There is no definite divid- 
ing line between the two divisions; predisposing causes may at 
times become exciting causes and vice versa, as when the ex- 
posure to extreme cold may directly cause necrosis or inflamma- 
tion, while a prolonged chilling may predispose to pneumonia, 
rheumatism, etc. In the main, however, predisposing causes 
form a class distinct from the determining causes, and in the 
great majority of instances, the body as a whole, or the part 

37 



38 GENERAL PATHOLOGY 

or parts subsequently affected, are first acted upon by the pre- 
disposing causes, preparing the tissues for the successful inva- 
sion or development of the real specific causative factors. 

Predisposing causes may be such biological conditions as sex, 
age, or race; or the predisposition may be acquired by previous 
disease, traumatism, injurious occupations, unsanitary surround- 
ings, bad habits of life, personal vices, etc., or again, such pre- 
disposition may be hereditary. 

Some of the principal predisposing causes may be briefly con- 
sidered: 

Age. — Children are especially liable to gastrointestinal disease 
because of the delicacy of these organs, and the abundance of 
lymphoid structures; to osteomyelitis, because of the vascularity 
of the growing bones ; to rickets, a nutritional disease involving 
principally but not exclusively the bones of the body; to diph- 
theria, whooping cough, measles, chicken pox, scarlatina, etc. 
Some of these diseases, particularly measles, are very contagious 
and confer life-long immunity, hence their prevalence in child- 
hood and their rare occurrence in later life. 

In adolescence certain physical and mental disorders and 
anemic conditions are apt to be met with. 

The "prime of life," from maturity to middle age, is on the 
whole probably the period most free from disease, still at this 
time occur those diseases which depend upon free association 
with other persons, upon exposure to inclement weather and to 
occupational hazards. After middle age incipient degeneration 
of the vital organs and tumors, particularly carcinomata, appear, 
while old age is subject to more pronounced organic changes and 
sclerotic conditions of the vessels and the trabecule of organs, 
predisposing to distinct visceral disease, apoplexy, etc. 

Sex. — Apart from the diseases peculiar to the different sexual 
organs of the male and female, men as a rule are more exposed 
to adverse climatic conditions, to dangerous pursuits, hence suf- 
fer from diseases liable to be favored by these predisposing fac- 
tors. Men, as a class, are also inclined to a far greater extent 
than women to indulge in excesses of all kinds, and are, there- 
fore, more subject to alcoholism, gout, and venereal disease, and 
to the great number of mental, nervous, and visceral pathologic 
changes which follow such diseases. 



ETIOLOGY OF DISEASES 39 

Race. — Some races are more susceptible to certain diseases, 
especially infectious diseases, than are others. The negro is 
relatively immune to yellow fever and malaria, probably because 
his tissues produce a greater number of antibodies due to sub- 
infections or the fact that his race has been exposed to such dis- 
eases for a longer time and to a greater extent than the white 
race. On the other hand, the negro is more susceptible to tuber- 
culosis. The American Indian and the Eskimo are free from 
tuberculosis in the native surroundings (lack of exposure?) but 
succumb readily to this disease when brought into civilized com- 
munities (due largely to lack of resistance — antibodies). The 
Japanese are said to be comparatively free from scarlet fever, the 
Chinese from cholera, while the Hebrew race is said to be more 
susceptible to diabetes than other races. 

Idiosyncrasy. — This is a marked susceptibility which certain in- 
dividuals have to the action of certain drugs, infections, foods, 
and even odors. The smallest doses of quinine will cause ex- 
tensive and painful eruptions in some persons ; the pollen of cer- 
tain plants will result in coryza and hay fever, or "pollen dis- 
ease." Strawberries, raspberries, lobster, and many foods give 
rise to urticarial eruptions in certain individuals. No satisfac- 
tory explanation of this individual hypersensitivity has yet been 
offered. A pronounced excitability of the nervous system may 
partly explain some cases, while in regard to idiosyncrasies to- 
ward drugs or chemicals it has been assumed that the cell con- 
stituents of the individuals affected contain atomic groups which 
readily combine with the substances. 

Traumatisms. — Injuries of all kinds act by causing shock and 
reducing the normal vital resistance. A fracture of the shoulder 
or other part of the body framework may predispose to pneu- 
monia; extensive burns lead to degenerations of the internal or- 
gans, etc. 

Injurious Occupations. — The inhalation of noxious gases predis- 
poses to respiratory and anemic disease; dust, particularly coal 
dust, leads to fibroid pneumonia and tuberculosis. Painters ab- 
sorb lead and suffer from intestinal derangements in consequence. 
Occupations requiring mental worry or prolonged and intense 
concentration have a marked depressing effect upon the general 
health. 



40 GENERAL PATHOLOGY 

Unsanitary Surroundings. — It must be self-evident that the 
health of individuals who dwell or work in buildings that are 
poorly ventilated, or that are located amid unclean or filthy sur- 
roundings, or in low, poorly drained sections, or where the in- 
mates are subjected to the dnst, smoke or fumes of large indus- 
tries, will be seriously affected and predisposed to disease. 

Habits. — Intemperance, whether in eating, drinking, use of to- 
bacco, use of drugs, sexual indulgence, etc., drains the human 
economy of its health reserve factors and makes it vulnerable to 
disease. Overwork and excessive play or recreation, in fact, ex- 
cess in any line of human activity should also be included in the 
term "intemperance." A proper variation of work and play, 
of mental or physical exertion and rest, is the only rule by which 
the normal health of the average individual may be conserved. 

Heredity. — Heredity is the transmission of certain characteris- 
tics or tendencies from parent to offspring. The maternal charac- 
teristics are present in the ovum, and the paternal in the sper- 
matozoon, the essential living parts of these parental elements 
being known as the germ plasm. Heredity therefore refers to the 
qualities contributed by either parent at the time of impregna- 
tion, and has nothing to do with conditions which may affect the 
health or development of the fetus during its life in utero. Thus 
certain diseases, as smallpox, measles, or syphilis, may be ac- 
quired by the mother subsequent to impregnation, and may be 
transmitted to the fetus through the placental circulation. The 
evidences of these diseases may be evident when the child is 
born, but they are not hereditary, but congenital, that is, dis- 
eases "acquired in prenatal life." It is usually held, however, 
that certain diseases, particularly syphilis, may also be trans- 
mitted through the germ plasm and, therefore, be hereditary, 
but as a rule it is merely the tendency to disease; i.e., the par- 
ticular impairment of health which favors the subsequent devel- 
opment of a certain disease, that is inherited, and not the dis- 
ease itself or its specific cause. As an example, tuberculosis may 
be given, for it is generally accepted at the present time that a 
lowered resistance or predisposition to tuberculous infection may 
be inherited, but not the tubercle bacillus. Diathesis is merely 
another term for an inherited predisposition to disease ; thus we 
speak of hemorrhagic, rheumatic or tuberculous diatheses. In 



ETIOLOGY OF DISEASES 41 

consanguineous marriages (marriages of blood relatives) the off- 
spring may suffer from an accentuation or "accumulation" of 
certain family weaknesses or diatheses. 

It will be seen that heredity is usually a predisposing factor, 
and only in a few instances (and these not admitted by all au- 
thorities) the direct cause of disease. 

Specific or Determining" Causes. — These may be physical or 
chemical agencies, living organisms or autointoxication. 

Traumatism. — Mechanical injuries, as blows, falls, knife or gun- 
shot wounds, etc., result in concussion, contusion, abrasion, lac- 
eration or rupture of the soft tissues, or fracture of the bony 
tissues. In all, except concussion, there occurs a certain amount 
of hemorrhage, which may be interstitial, as in contusions, or 
external, or into natural body cavities. Disintegration of the 
blood and injured tissues results with more or less inflammation. 

Concussion is the violent jarring of an organ, accompanied 
by slight, profound, or fatal shock', but unaccompanied by visible 
changes in the structure of the organ. In concussion of the brain, 
the vital centers are excessively stimulated by the blow, then 
depressed, or in fatal cases, paralyzed. Contusion (or bruising) 
and laceration may be, and often arc. associated with concus- 
sion, but are not essential features of the latter. 

Sltock is a depression of the vital centers, particularly the car- 
diac and respiratory centers, resulting in weakened heart action, 
irregular breathing, lowering of the bodily temperature, pallor, 
and clamminess of the skin. Shock may be caused by an injury, 
or by a strong emotion, as great fear, acting upon the nerve 
centers. 

Pressure upon a part, if continuous, will result in atrophy. In- 
termittent pressure will cause atrophy of some of the constituents 
of the tissues affected, and hyperplasia of others, particularly the 
connective tissues. 

Heat. — A moderate excess of heat, locally applied, will cause 
hyperemia; a higher degree will cause, in addition, necrosis, par- 
ticularly vesication (liquefaction necrosis). A still higher de- 
gree of heat will char or burn the tissues, with oxidation of the 
superficial parts and necrosis of the deeper parts. Burns which 
cover one-third of the surface of the body are nearly always 
fatal, due to absorption of toxic products formed in the burned 



42 GENERAL PATHOLOGY 

tissues, and to the fact that a large part of the eliminating sur- 
face of the skin is destroyed. In severe cases death is due to 
shock. 

First degree burns are those that are characterized by swelling 
and reddening of the skin; second degree burns, by the forma- 
tion of vesicles (or blisters) and bullae; third degree barns, by 
destruction of all the layers of the integument with more or less 
of the subcutaneous tissue and ulceration. The burns so de- 
scribed refer only to burns of the skin. 

Burns may proceed deeply into the tissues (sometimes called 
fourth degree burns) with coagulation of the cells and other 
forms of necrosis and oxidation, until in fact the whole body is 
incinerated (completely oxidized). 

Sunstroke may be caused by exposure to the heat of the sun. 
The bulbar heat centers are depressed or paralyzed by the heat, 
or metabolic poisons are formed by the heat which act upon the 
centers, resulting in very high temperatures (107° to 112°) with 
labored breathing, headache, vertigo, nausea, delirium and finally 
coma. 

Heat exhaustion results from high temperature with humidity, 
or less often from exposure to the sun alone. This is probably 
due to vasomotor paralysis, and the symptoms are those of col- 
lapse with subnormal temperature ; rapid, weak pulse ; rapid, 
shallow breathing ; and livid color. 

Cold. — The primary effect of cold to the surface is contraction 
of the superficial capillaries causing the parts to appear blanched 
and anemic. Soon the vasoconstrictors are paralyzed, the ves- 
sels dilate, and the parts become swollen and livid and more or 
less painful {frostbite). In a severe frostbite the part becomes 
covered with vesicles, the blood plasma coagulates with disinte- 
gration of the blood cells and thrombosis of the vessels ; gangrene 
may or may not follow. Unless gangrene sets in, recovery takes 
place, but in many cases chilblain, or pernio develops as a secon- 
dary effect of frostbite. This is a condition in which swelling 
and pain or tingling sensations return in a previously frostbitten 
part upon approaching a fire, upon exercising, or exposure to 
slight cold. Repeated attacks lead to vesication and ulceration. 

Excessive cold will coagulate the cells and fluids of a part, 
with subsequent gangrene. Sudden exposure to very low tern- 



ETIOLOGY OF DISEASES 43 

peratures produces lesions practically identical with those caused 
by burns. 

Atmospheric Pressure. — Increased atmospheric pressure causes 
the tissues and fluids to hold more gases (almost exclusively 
nitrogen), and subsequently when the return to normal pressure 
is too sudden, bubbles of gas appear in the tissues and blood ves- 
sels. At first these bubbles are located only in the capillaries, 
which may rupture with interstitial hemorrhage, bleeding from 
mucous surfaces, as nose, accompanied by symptoms of nausea, 
palpitation of the heart, prostration, delirium and palsies. The 
tiny bubbles may coalesce into larger ones and form air emboli, 
or gas emboli, which are apt to be fatal. At necropsy congestion 
of the central nervous system and thoracic organs have been 
found, with hemorrhages into the meninges and vacuolization of 
the spinal cord. This condition is called caisson disease. 

Decreased atmospheric pressure causes vascular and nervous 
disturbances, with apparent increase of the red blood cells and 
hemoglobin due to the escape of the plasma into the tissues (rel- 
ative polycythemia). The symptoms may be due to lack of 
oxygen, together with the mechanical effect of decreased pres- 
sure upon the tissues. This condition is sometimes called moun- 
tain disease. 

Electricity. — Powerful electrical currents usually kill by pa- 
ralysis of the heart. The local effects may be demonstrable or 
not, according to the nature of the conductors and the parts 
affected, as well as the intensity and duration of the current. 
Frequently there are burns, which may be deep and dry; the 
brain and meninges are congested, and there may be minute 
hemorrhages into the gray matter, floor of the fourth ventricle, 
and other parts, with congestion of the thoracic and abdominal 
organs. Lightning strokes often cause peculiar branching linear 
burns upon the skin; and the clothing, and particularly the foot 
wear, may be torn into shreds, and even internal organs have 
been found to be lacerated. 

Light. — Light is usually regarded as beneficial to the health 
of the higher organisms, but it is harmful to unicellular organ- 
isms, as bacteria; in fact sunlight is bactericidal. Strong sun- 
light may cause hyperemia or inflammation of the skin {sunburn), 



44 GENERAL PATHOLOGY 

which, if severe, may proceed to vesication and ulceration. In- 
tense light of any kind, as calcium light, may cause retinitis. 

X-rays. — X-rays cause degenerative changes in the cells, and 
finally disintegration. The cells of diseased tissues are more 
easily destroyed than healthy cells. Chronic dermatitis with a 
tendency to epitheliomatous change is apt to follow x-ray burns 
of the skin. Highly specialized cells, as spermatozoa, are readily 
destroyed by exposure to these rays. 

Chemical Agents. — Any substance which by its chemical ac- 
tion destroys (corrodes) tissues, or which, when absorbed and 
carried to various cells, causes harm, is called a poison. A sub- 
stance may be a therapeutic agent as well as a poison, depending 
upon the amount introduced into the tissues. One-fortieth of a 
grain of arsenic is a stimulant to the nervous system and the 
hematopoietic organs, and therefore a useful tonic, but one or 
two grains will cause death. 

The study of poisons is too extensive a subject to be under- 
taken, even in a summary manner, in a work of this kind, and 
the reader is referred to works on toxicology for their further 
consideration. 

Living Organisms. — Living organisms are the most important 
direct causes of disease, and will be considered in Chapter VIII. 

Autointoxication, or self-poisoning, is a diseased condition 
caused by the accumulation in the tissues of an abnormal amount 
of normal waste products, as a result of impaired elimination, 
or by the formation of abnormal, toxic substances, as a re- 
sult of impaired metabolism, or impaired gastrointestinal di- 
gestion. Poisoning due to the mere absorption of products of 
intestinal putrefaction is not included in this term. 



CHAPTER III 

PATHOLOGIC PROCESSES 

All pathologic processes are either (1) simple — those in which 
the changes are of one kind only, as in atrophy, or (2) compound 
— those in which two or more simple processes are taking place 
at the same time, as in inflammation. 

Pathologic processes may also be divided into (a) progressive, 
in which tissues are built up, and (b) retrograde or retrogressive, 
in which tissues are broken down. 

RETROGRADE PROCESSES 

Atrophy 

Atrophy is a simple retrograde process, resulting in the de- 
crease in size of a part or an organ. Normal examples are the 
atrophy of the thymus gland after the first few years of child- 
hood, of the uterus after parturition, of the overies after the 
menopause. 

Atrophy may be divided into simple atrophy, which is a de- 
crease in the size of the cells, and numerical atrophy, a decrease 
in the number of the cells. More often these two types are as- 
sociated or combined, hence sometimes called combined atrophy. 
Simple atrophy when unaccompanied by any other pathologic proc- 
ess is a true atrophy, while numerical atrophy, in which the cells 
are usually first degenerated (hence degenerative atrophy), is usu- 
ally accompanied by a replacement of the destroyed cells by 
fatty tissue or a hyperplasia of connective tissue, making it ex- 
tremely difficult to distinguish between atrophy and degenera- 
tion with replacement. 

The term "atrophy" usually refers to local atrophy (affecting- 
one or more parts) while atrophy of all, or nearly all parts of the 
body (emaciation) is sometimes called general atrophy. Hypopla- 
sia, infantilism, nanism, ateleiosis, etc., are terms referring to va- 
rious forms of underdevelopment or stunted growth, and must not 

45 



46 



GENERAL PATHOLOGY 



be confounded with atrophy. Aplasia or agenesia means total lack 
of development of a part. 

Etiology. — The causation of normal atrophy is not well under- 
stood, but pathologic atrophy is due to diminished nutrition of a 
part, depending upon : 

1. Prolonged, continuous pressure ("pressure atrophy," as by 
tumors, aneurysms, corsets, etc). 

2. Disuse, as in fractures, paralysis, habit, etc. 

3. Loss of trophic influence, as, in muscular atrophy due to 
disease of the spinal cord (neuropathic atrophy). 

4. Starvation, general or local, as from obstructed blood vessels. 

5. Senility, affecting especially the heart, lungs, liver, kidneys, 
testicles, uterus and bones. 

Locations. — Any part of the body may become atrophied. 




Fig. 3. — Brown atrophy of the heart muscle. (Stengel and Fox.) 



Gross Morbid Anatomy. — In true atrophy, the part or organ 
is diminished in size withoiit change in shape or consistence. In 
the degenerative type, the shape is usually much altered, the 
size unaltered or decreased, and the consistence increased, or de- 
creased according to the nature of the tissue which has re- 
placed the atrophied cells. In both forms the color is usually 
increased, becoming darker, from a relative or absolute increase 
of pigment. 

Pathologic Histology. — In true atrophy the cells are smaller 
than normal, and pigment granules can usually be seen. In 
brown atrophy of the heart, these granules are arranged about 
the poles of the more or less elongated nucleus (Fig. 3). In 
numerical atrophy, the parenchymatous cells are smaller, fewer 
in number, and in places altogether absent, and in their stead 



PATHOLOGIC PROCESSES 



47 



may be seen connective-tissue elements, hyaline, fatty or mucoid 
material, and some type of pigmentation. 

Pathologic Physiology. — Since the parenchyma of organs is 
chiefly though not exclusively affected, function is always im- 
paired — secretion diminished, muscular activity lessened, etc. 

Results. — If the process is arrested early, partial or complete 
restoration may be attained ; if not, death of the part will result 
with its disappearance and replacement by other tissue. 

Degenerations (or Metamorphoses) 

Degenerations are simple retrograde processes in which the 
cells or the intercellular substances are converted into a ma- 
terial abnormal in kind or quantity. 

ftj&g 2 ^T 

J 




Fig. 4. — Albuminous degeneration — kidney. (Delafield and Prudden.) 

There are six types of degeneration: 

Cloudy swelling, or parenchymatous or albuminous degenera- 
tion. 

Fatty degeneration. 

Mucoid or myxomatous degeneration. 

Colloid degeneration. 

Hyaline degeneration. 

Amyloid degeneration. Whether amyloid is an infiltration or 
a degeneration can not be definitely stated — even its chemical 
composition is not yet definitely determined (see Etiology of 
Amyloid Degeneration). 



48 GENERAL PATHOLOGY 

Cloudy Swelling, Parenchymatous or Granular Degeneration 

Cloudy swelling is a simple retrograde process in which the 
soluble albuminous elements of the cells are precipitated as in- 
soluble granules, associated with an increase of fluids in the cells. 
(Fig. 4.) 

Etiology. — Cloudy swelling is caused by the action of poisons, 
as (a) toxins of infectious diseases, particularly scarlet fever, 
diphtheria, and typhoid fever, (b) extraneous poisons, as ether, 
chloroform, mercury, etc.; and (c) poisons formed within the 
body, as in autointoxication, the metabolic disturbances accom- 
panying high temperature (pyrexia), absorption of necrotic tis- 
sue or disintegrating materials, etc. 

Locations. — Chiefly the parenchyma of organs, particularly 
renal epithelium, mucous membranes, liver cells, voluntary mus- 
cle and heart. 

Gross Morbid Anatomy. — The organ is uniformly enlarged, 
owing to the swollen conditions of the cells; paler than normal, 
due to the whiteness of the granules and the anemia caused by 
the pressure of the swollen cells; softer, owing to the increased 
fluid content. On section the surface is moist and the parenchyma 
protrudes. 

Pathologic Histology. — The cell is full of fine granules, which 
partly or wholly obscure the nucleus and the striations of muscle 
fibers. The cells are increased in size and more or less irregular 
in outline. The cell Avail is sometimes indistinct, causing the cells 
to have the appearance of having coalesced. 

Reactions. — The granules may be dissolved in acetic acid, thus 
causing the reappearance of the nuclei, but they are insoluble in 
alcohol or ether, thus differentiating them from fat globules or 
granules. 

Pathologic Physiology. — Function is impaired due to the pres- 
ence of the granules and the intracellular fluids. 

Results. — Granular degeneration is a temporary condition oc- 
curring in acute disease, and complete recovery is the rule, but if 
the causes persist, fatty or other degeneration ensues. 

Fatty Degeneration 

Fatty degeneration is a simple retrogressive process in which 
there is disintegration of the cellular protoplasm, with appearance 



PATHOLOGIC PROCESSES 49 

of fat within the cell. Normal examples are the production of 
fat globules in the secretion of milk, and the change of red 
(fetal) to yellow (adult) bone marrow. (Fig. 5.) 

Etiology. — Since cloudy swelling may pass into fatty degenera- 
tion, the prolonged action of toxins and poisons which cause the 
former will also cause the latter. Fatty degeneration also oc- 
curs in pernicious anemia and in cachexias, due to some form of 
toxin; and in the involution of tissues, as thymus, corpora lutea, 
uterus, etc. 

Locations. — Fatty degeneration occurs in the parenchyma of 
organs, and at times also in the connective tissues, as in athero- 
matous vessels. 

Gross Morbid Anatomy. — The organ is smaller (though in early 



1 
Ik 




:' . " ■• .- * 

it v : •■ ' • • »; 



-" m*mk 



Fig. 5. — Fatty degeneration — kidney. (Delafield and Prudden.) 

stages it may be enlarged) and softer than normal. The color 
is pale yellow, due to the presence of fat, but congestion, pigmen- 
tation, or jaundice may alter the color. The specific gravity is 
reduced. The area affected may be uniform or the degeneration 
appear in streaks, as in the heart and liver, thus producing a 
mottled appearance. On section the knife becomes greasy. 

Pathologic Histology. — The cells are in the early stages usually 
somewhat larger than normal, but later are shrunken, irregular 
in shape, and more or less degenerated as shown by their di- 
minished staining qualities. The cells are partly or in later 
stages completely filled with small, discrete, highly refractile 
fatty granules, scattered irregularly throughout the cytoplasm. 
In acute or very advanced cases these fat granules may coalesce 
into globules, which in exceptional cases may become quite large. 



50 GENERAL PATHOLOGY 

At first the nucleus is not affected, but in late stages of the dis- 
ease it shows degenerative changes (karyolysis). Cells crowded 
with fat granules are sometimes called "compound granule 
cells." 

Pathologic Chemistry. — In fatty degeneration, the cells are first 
degenerated by the poisons indicated in describing its etiology, 
followed in the main by an infiltration of fat from without. In 
the kidneys, spleen, and muscles, 1 hoAvever, the fat is formed 
principally by the setting free of the intracellular fat from its 
combination with the protein substances by autolysis, i.e., the fat 
previously present but invisible is rendered visible. 

Reactions. — Fat is soluble in alcohol, ether, and chloroform; 
but is not dissolved by acetic acid. It is stained red by Scharlach 
E, and orange by Sudan in. Osmic acid stains fat a deep black, 
due to the olein present in all natural fats. 

Pathologic Physiology. — Impairment and finally destruction of 
the secreting or muscular functions (as in heart muscle) result. 
In the liver and kidney secretion, however, is well maintained 
even in advanced cases. 

Results. — Mild cases with uninvolved nuclei may recover, but 
the condition is generally irremediable, the degeneration pro- 
ceeding to complete death of the cells (necrobiosis) with depo- 
sition of fatty acid crystals, cholesterin, etc., or the damaged tis- 
sue may undergo calcification. 

Mucoid Degeneration 

Mucoid degeneration is a simple retrogressive process in which 
there is a conversion of the cells or intercellular substance into 
some type of mucin. Normal examples are the secretions of the 
goblet cell of the mucous membrane, and Wharton's jelly of the 
umbilical cord. (Fig. 6.) 

Etiology. — The causes which bring about this form of de- 
generation are not definitely known. Inflammation is a factor 
when mucoid degeneration appears in mucous membranes. 

Locations. — (a) Mucous membrane, affecting the columnar cells, 
resulting in the formation of a large number of goblet cells, (b) 
Intercellular substance of subcutaneous, subserous and submucous 



nVells, II. Gideon, Chemical Pathology, Philadelphia, W. B. Saunders Co. 



PATHOLOGIC PROCESSES 



51 



tissues, either as a diffuse process (myxedema), or as a local 
process in nasal polyps, hydatiform moles, etc. (c) In tumors, as 
ovarian cysts, carcinoma springing from mucous membranes (the 
so-called "colloid cancers"), myxomata, etc. 

Gross Morbid Anatomy. — The mucous membranes are covered 
with a viscid semigelatinous and colorless material, while in the 
antrum of Highmore, salivary glands, etc., there are cyst-like col- 
lections of the same material. When affecting the connective 
tissues, these are soft, elastic and tear easily. In tumors the 
mucoid material is drier; in ovarian cysts the material may as- 
sume large proportions. 




m 



j 



Fig. 6.- — Mucoid degeneration of fibrous tissue. (Delafield and Prudden.) 



Minute Morbid Anatomy. — The cells are partly or completely 
filled with the mucus; the typical "goblet cells" are distended 
and the nucleus pressed to one side. The material is usually 
homogeneous, but in connective tissues it may appear as granules 
or as coarse shreds lying between the cells; the cells present all 
stages of degeneration from the normal appearance to typical 
mucoid cells, with irregularly stellate outline. 

Pathologic Chemistry. — Mucin is a compound protein (giuco- 
samin), normally secreted by the epithelium of mucous mem- 
branes, and also occurring in the mucoid tissue of the fetus, 
where it is the precursor of the adult connective tissue. The 
mucoid degeneration associated with inflammation of mucous 
membranes (catarrhal inflammation) is in reality only a path- 



52 GENERAL PATHOLOGY 

ologic increase of mucinous secretion of epithelial cells, which is 
essentially true also of this substance in "colloid cancers" and 
ovarian cysts; the pathologic connective-tissue mucin is merely 
a reversion to the fetal type of connective tissue. In ovarian 
cysts this product differs somewhat in chemical properties from 
true mucin, hence called pseudomucin. 

Reactions. — Mucin swells in water, dissolves in alkalies, is in- 
soluble in acids and alcohol, and is precipitated by acetic acid. 
It is acid in reaction, hence takes the basic stains. Pseudomucin 
is not precipitated by acetic acid, is alkaline in reaction, and 
takes the acid stains. 

Pathologic Physiology. — Function is moderately impaired in 
mucous membranes, resulting in catarrhal conditions. In connec- 
tive tissues, the change is apt to be permanent but usually causes 
no serious harm. 

Colloid Degeneration 

This is a simple retrograde pathologic process in which there 
is a conversion of the cell into a yellowish brown transparent ma- 
terial, resembling in physical appearance the colloid material of 
the thyroid gland. (Fig. 7.) 

Pathologic Chemistry. — The colloid of the thyroid is an iodin- 
containing globulin, but the term as used in "colloid degenera- 
tion" is not chemically definite, bnt includes such substances as 
have a colloid appearance (just described). "Colloid cancer" 
was so named because the mucoid material found within it had 
a colloid appearance, due to its compression within a confined 
space, and to its partial loss of water. Apart from that found in 
the thyroid, colloid resembles the mucins in chemical composi- 
tion, particularly pseudomucin. 

Etiology. — The etiology is obscure. Pathologically it is partly 
a secretion and partly a degeneration of the epithelial cell. 

Locations. — It occurs in goiters and other tumors of the thyroid 
gland, in the hypophysis cerebri, kidneys, adrenals, prostate 
gland, and seminal vesicles, and many other locations. 

Gross Morbid Anatomy. — The organs affected may be larger, 
and either harder or softer than normal. The colloid substance 
occurs in cystic collections, having a yellowish brown transparent 



PATHOLOGIC PROCESSES 



53 



appearance, varying in size from minute bodies to large masses, 
having the consistence of calf's foot jelly. A serious transuda- 
tion may dissolve the colloid, leaving cavities filled with choco- 
late-colored fluid. 

Pathologic Histology . — The material first appears in the epi- 
thelial cells as droplets ; the latter become completely trans- 
formed into colloid, and as new layers of cells are formed and 
successively degenerated, the acini, tubules or cystic cavities 
formed to receive the material, become distended to various de- 
grees. The substance is usually homogeneous in appearance, but 
may show concentric lines corresponding to the layers of cells 
which have undergone the change. 




k 



/.<• ¥-•:;:.. Hit. 



&H2 
3? 



.y» 



••, 



k.-v 






'**»i 






if 



• » 



%r** 




k v; 



Fig- 7. — Colloid degeneration of the thyroid gland showing masses of colloid matter in 
the gland acini. (Karl and Schinorl.) 



Reactions. — Colloid does not swell in water ; is not precipitated 
by acetic acid, but is precipitated by tannic acid. Like pseudo- 
mucin, it elects the acid dyes, but the more nearly it approaches 
the mucins in composition, the more variable are its staining 
properties. 

Pathologic Physiology. — Function is impaired, probably on ac- 
count of the pressure to which the vital elements are subjected 
by the material. 

Results. — Absorption with regeneration of epithelial cells is 
possible in some cases. When the process has caused destruction 



54 GENERAL PATHOLOGY 

of considerable amounts of parenchymatous cells, colloid de- 
generation is usually followed by hyaline mucoid, necrotic or 
calcareous change. 

Hyaline Degeneration 

Hyaline degeneration is a simple retrograde morbid process 
with the appearance in the cells and intercellular substance of a 
homogeneous, glistening, opaque, albuminous material, called 
hyaline (glass-like). (Fig. 8.) 

Pathologic Chemistry. — This material is closely related to col- 
loid and amyloid substances, being distinguished mainly by its 




Fig. 8. — -Hyaline degeneration of an ovarian capillary. Oc. 2; ob. 9. (McFarland.) 

physical properties and its distribution. Hyaline is not a chemical 
entity, but includes a number of different chemical substances, 
i.e., various forms of degeneration or necrosis. 

Etiology. — The causal factors are not well understood. Ar- 
teriosclerosis, and all forms of arteritis favor its production ; also 
the toxins of infections (chiefly the acute infections, as scarlet 
fever) and septic processes, lead poisoning, etc., but chronic in- 
fectious disease, as tuberculosis, syphilis, etc., may also be fol- 
lowed by this change. 

Locations. — It may be found in any part of the body, but there 
are three principal types: (a) Connective-tissue hyaline, found 



PATHOLOGIC PROCESSES 55 

in dense tissues, as old scars, sclerotic vessel walls, capsules and 
trabecule of organs, especially of the spleen, liver, heart, brain, 
cord, etc. 

Von Recklinghausen's hyaline is that which involves the cap- 
sules and trabecule of lymph nodes, especially when the seat of 
tuberculosis. 

(b) Cellular hyaline, occurring as round bodies within cells, 
such as epithelium of mucous membranes and the kidneys. Zen- 
ker's hyaline occurs in voluntary muscle cells, as the rectus ab- 
dominis, diaphragm and adductors of the thigh in typhoid fever, 
though some believe this to be amyloid degeneration, others, a 
form of coagulation necrosis. 

(c) Necrotic hyaline, found in old blood clots (hyaline 
thrombi), in fibrinous and inflammatory exudates (exudative hy- 
aline), and in necrotic tumors, tubercles, gummata, etc. 

Eussell's " fuel i sin bodies" are small round hyaline bodies, con- 
centrically striated, found within and between cells of epithelial 
tumors, and sometimes in normal tissues. Their true nature is 
not known, but they resemble hyaline material in appearance and 
in affinity for acid fuchsin stains. 

Gross Morbid Anatomy. — Hyaline is not usually sufficiently 
abundant to be seen by the naked eye, but when so, it appears 
similar to hyaline cartilage, is smooth, and cuts with the same re- 
sistance. In mucous and serous membranes, small collections 
may appear as opaque irregular plates. 

Pathologic Histology. — (a) In the blood vessels hyaline is seen 
in and beneath the endothelium as a homogeneous material, also 
between the vascular coats, or around the vessels (such perivas- 
cular hyaline is especially well seen in cylindromata). The ves- 
sel wall is thickened, the lumen narrowed, and possibly ob- 
literated, (b) In interstitial tissues, hyaline material is found 
between the muscle fibers, hepatic cells, renal tubules in the 
reticulum of lymph glands, in the retina, in cicatrices, and in 
neoplasms, (c) Within cells, hyaline material occurs as homo- 
geneous bodies in muscle cells, giant cells, epithelium, and to a 
lesser extent in leucocytes and wandering cells. 

Reactions. — Hyaline is resistant to reagents, being unaffected 
by acids, alkalies, and alcohol. The staining reactions are varia- 
ble, owing to its variable composition, but usually hyaline ma- 



56 



GENERAL PATHOLOGY 



terial has a decided affinity for acid fuchsin, and other acid 
stains; but the older the hyaline, the paler it stains. Thionin 
stains it red and other tissues blue. 

Pathologic Physiology. — Hyaline degeneration does not impair 
function as a rule ; but if it is extensive, it may affect the paren- 
chyma by compression or by anemia through narrowed blood ves- 
sels. 

Results. — It may be absorbed, or converted into fatty degenera- 
tion, or undergo caseation or calcification. 



Amyloid Degeneration (Waxy, Bacony, or Lardaceous 
Degeneration) 

Amyloid degeneration is a simple retrograde process with the 
appearance in the intercellular substance of connective tissues of 
a waxy albuminous material, called amyloid. (Fig. 9.) 




Fig 9. — Amyloid infiltration of capillary walls in kidney glomerulus. (Stengel and Fox.) 

Pathologic Chemistry.— This substance was at first thought to 
be a form of cellulose because it gave the blue color with iodine 
when followed by sulphuric acid, and was hence called ''amy- 
loid" or starchlike, but is now believed to be a protein combined 
with chondroitin-sulphuric acid; though Hansenn failed to find 
any of the latter in amyloid of the spleen, thus making the chem- 
istry of amyloid material doubtful. 



PATHOLOGIC PROCESSES 5/ 

The material may be carried by the blood in a "preamyloid" 
soluble form to the tissues, where it is modified and deposited, be- 
coming the insoluble resistive amyloid substance, though it is 
possible that in some localities it may be formed in situ; hence 
it is variously called an ''infiltration" or a "degeneration." 

It will be noted, then, that the chemical nature of the four 
"albuminous degenerations;" viz., mucoid, colloid, hyaline, and 
amyloid, is not definitely known, and probably varies much in 
different cases. 

Etiology. — Toxins of certain chronic infectious processes, espe- 
cially those formed in prolonged suppurating conditions (particu- 
larly tuberculous and syphilitic) of bones, though suppurative 
and ulcerative conditions of various kinds, as gastrointestinal, 
actinomycotic, etc., may also cause amyloid degeneration. 

Aseptic suppuration, as by injection of turpentine, may also 
cause it. 

The injection of toxins alone, as in preparation of diphthe- 
ritic antitoxin, and the toxins of nonsuppurative syphilitic condi- 
tions likewise cause it. 

It sometimes occurs without apparent cause. 

Locations. — The condition may be general (amyloidosis) or lo- 
cal. The organs most frequently affected are the kidney, liver, 
and spleen; next in frequency, the larger blood vessels, intestinal 
mucosa, and lymph nodes, and less frequently the stomach and 
colon, suprarenals, pancreas, heart, etc. ; rarely the lungs or cen- 
tral nervous system. 

Gross Anatomy. — An amyloid organ is enlarged uniformly (oc- 
casionally an amyloid liver becomes enormous) dense, pale, in- 
elastic or doughy, sometimes pitting on pressure. The specific 
gravity is increased. 

The amyloid material has a glistening, waxy, translucent ap- 
pearance. In cut sections, the surface is smooth, dry and glossy, 
the cut edges remain sharp, and the parenchyma neither con- 
tracts nor protrudes. It is customary in examining gross speci- 
mens at autopsy to apply iodine (Lugol's). 

The waxy material is not always uniformly distributed; in 
the spleen it may be confined to the Malpighian bodies, which 
stand out in round, transparent bodies, looking like grains of 
boiled sago (sago spleen); when the process is diffuse, the spleen 



58 GENERAL PATHOLOGY 

looks bacony (baeony spleen). In the kidney, it appears first 
in the glomeruli. 

Pathologic Histology. — The material is always found in the 
connective tissue; is usually found in the capillaries, in the media 
and basement membrane of intima in case of larger vessels ; the 
lumen of the blood vessels is usually narrowed or obliterated. 
The amyloid material is deposited between the cells, which are 
pushed aside and atrophied, and disappear as the process ad- 
vances. The amount of amyloid substance varies from slight 
deposits to such large quantities as to cause disappearance of 
the original elements from large areas of the diseased part. 

Under the microscope, the amyloid in a section of liver is 
found in the intermediate zone of the lobule (i.e., between the 
central and perilobular zones) as a pale homogeneous material 
following the course of the capillaries, and taking the charac- 
teristic stain ; from this zone it gradually spreads until the whole 
lobule is affected. 

In the kidney, the capillary tufts are first affected, later the 
vessels and interstitial tissues ; rarely the tubules are said to 
contain it, though in most cases this material is hyaline or 
other exudative material and not true amyloid. 

In the spleen, the Malpighian bodies alone may be affected, 
or the reticular framework may be generally involved. 

Reactions. — Amyloid is insoluble in water, acids, alkalies, and 
very resistant to bacterial decomposition. 

It stains a deep mahogany broAvn with iodine, other tissues, 
yellow; if afterward treated with dilute sulphuric acid, it usu- 
ally turns brown or blue, or may merely turn a deeper brown. 
This iodine reaction fails in specimens that have been kept some 
time in preserving fluids, or that have become strongly alkaline ; 
in fact, the blue reaction is usually given well only by splenic 
amyloid, or by the "amyloid bodies." 

Gentian violet, or methyl violet (and to a less degree also 
other basic aniline dyes) stain the amyloid material a pink color, 
or pale red often with a violet tinge ; the other tissues stain the 
natural violet color. 

Pathologic Physiology. — No impairment of function occurs if 
the material is small in amount ; if large, pressure causes atrophy 
and diminished function, or thrombosis in the blood vessels. 



PATHOLOGIC PROCESSES 59 

Results. — The process is irremediable; and if progressive, leads 
to death. It may also pass into fatty degeneration, caseation, 
or calcification. Slight amormts may be absorbed, learned by ex- 
perimentally extirpating a part of a diseased (amyloid) area of 
an organ, and some time afterward again examining at necropsy. 

The "amyloid bodies," or corpora amylacea, fonnd in the pros- 
tate, lungs, kidney, brain, and posterior cord, also sometimes in 
inflammatory areas, in infarcts, granulomata. and neoplasms, are 
small concentrically striated bodies, resembling starch granules, 
which nearly always react with the iodine-sulphuric acid, giving 
a blue color, though sometimes they fail to react typically. Many 
believe these bodies to be hyaline, others colloid in nature. Path- 
ologically they are not significant, occurring also in health. 

Infiltrations 

Infiltrations are simple retrograde processes in which there is 
deposited within the cells and intercellular tissues substances 
that are abnormal in kind or quantity. 

Fatty Infiltration 

Fatty infiltration is an abnormal deposition of fat within the 
cells of a part. The process does not differ essentially from the 
normal physiologic deposit of fat. and is considered pathologic 
only when in excess or when deposited where it does not normally 
appear. (Fig. 10.) 

Etiology. — 1. Ingestion of more fat-forming foods — fats and 
carbohydrates — than the body needs. 

2. Sulfoxidation probably accounts for nearly all, if not all, 
the remaining cases, as in tuberculosis, carcinoma, inactivity, 
senility, alcohol, diabetes, etc. 

Types. — 1. General fatty infiltration, as obesity, adiposity or 
polysarcia. 2. Local fatty infiltration, as in heart, etc. 

Locations. — 1. Connective tissues; (a) General deposits, as in 
subcutaneous, submucous and subserous tissues. Obesity, belongs 
here. Tissues that are never involved are the eyelids, ears, alse, 
nasi, lips and external genitals. Tissues rarely involved are the 
lungs and central nervous system, (b) Local deposits — found 
usually along the fascia? and trabecular lines of parts or organs, 



GO 



GENERAL PATHOLOGY 



as heart, kidney, pancreas, old necrotic foci, degenerated or 
sclerosed organs, etc. 

2. Glandular epithelium — practically limited to liver cells. "In 
liver the connective-tissue cells are not involved, but the liver 
cells. In all other parts of the body, the connective tissue cells 
are involved." — Adami. 

Gross Anatomy. — The part or organ is enlarged (sometimes 
double), tense, and elastic, yellow in color which may be modified 
by other factors and the sharp edges rounded. 




>4K 

10. — Fatty infiltration of the liver. 



(Stengel and Fox.) 



Section may show minute fat droplets, and present a uniform 
yellow surface; or yellow streaks as is usually the case in fatty 
infiltrated heart. 

Pathologic Histology. — Large globules appear in the cells of 
connective tissues, or in hepatic cells. The protoplasm is usually 
clear and of normal appearance. The nuclei stain well, showing 
that they are not involved, but they, as well as the protoplasm, 
are apt to be pushed to one side of the cell, giving the "seal- 
ring" or "signet-ring" appearance. The cell wall is distinct, 
and often bulged. 

In the liver, the infiltration begins in the cells at the periphery 
of the lobule, and proceeds toward the center as the process ad- 
vances. 

Reactions. — They are the same as in fatty degeneration. 



PATHOLOGIC PROCESSES 61 

Pathologic Physiology. — Function is not impaired except when 
infiltration is extensive enough to cause pressure. 

Results. — Recovery takes place by absorption, if the infiltration 
is slight or even moderate. If extensive or of long standing, it is 
followed by fatty degeneration or necrosis. 

Table of Differences Between Fatty Infiltration and Fatty 
Degeneration 

Fatty Infiltration Fatty Degeneration 

Deposit of fat in healthy cells. Deposit in diseased cells. 

Globules of fat usually large. Globules usually small. 

Nuclei uninvolvcd, staining well. Nuclei involved, staining poorly. 

Cytoplasm healthy and capable of Cytoplasm degenerated, 
resuming function if fat be ab- 
sorbed. 

Nucleus and cytoplasm apt to be Nucleus not displaced, 
pushed to one side — " signet ring." 

Condition not necessarily serious. Always serious. 

Pigmentary Infiltration 

Pigmentary infiltration is an abnormal deposit of pigment 
within or between the cells of any tissue. 

Etiology. — I. Extraneous pigments (those of external origin) 
are derived from: 1. Inhalation of smoke and dust particles of 
all hinds, causing pneumonokoniosis or "lung dust disease." 

2. Ingestion of dust and substances like soluble salts of silver, 
especially the nitrate, also lead salts, etc. 

3. Implantation and absorption by skin, as in tattooing, and 
possibly lead, copper, etc. 

II. Pigments of internal origin are due to: 

1. Disintegration of hemoglobin (hemolysis) either directly in 
the tissues, or in the blood vessels when the blood is hemolyzed 
by venins, toxins, poisons, anemias, cachexias, etc., (hematog- 
enous pigmentation) ; or indirectly, when the blood pigment is 
converted into bile pigment in the liver, but instead of escaping 
as normally through the hepatic ducts with the bile, should these 
ducts become obstructed by catarrhal or other conditions, the 
bile pigments are forced into the lymph vessels (and to a less 
extent into the blood vessels) and carried to the tissues through- 
out the bod}^ (hepatogenous pigmentation). 



62 GENERAL PATHOLOGY 

2. Malarial pigmentation. This is probably formed by the ac- 
tion of the Plasmodium malarias upon the red blood cells, liberat- 
ing and modifying the hemoglobin or hematin. 

3. Metabolic pigmentation. Certain cells elaborate the pig- 
ment out of protein substances possibly by action of intracellular 
oxidases upon the aromatic groups of the protein molecule (von 
Furth's theory). 

Such pigment appears normally in skin, hair, choroid and 
retinal coats of the eye, in pregnancy (chloasma uterinum) and 
pathologically in certain tumors, in the skin, etc. 

The term melanin is applied to all these pigments though they 
vary much in composition, some being iron or sulphur free, while 
some contain small amounts of iron, and some contain sulphur 
in variable amounts up to 10 per cent in melanosarcomata. 

Lipochromes, or pigments of fatty origin, are usually classed 
as metabolic pigments, but their nature and formation are not 
well understood; they occur normally in fats, in the corpora 
lutea (lutein) and pathologically in lipomata, xanthomata, (pale 
yellow), in chloromata (green), in certain nerve cells in old age, 
and possibly in brown atrophy of muscle cells (but this has also 
been classed as hematogenous in origin.) 

4. Parasitic pigmentation. Some bacteria and moulds form 
various pigments. 

Locations. — Much of the inhaled pigment probably never 
reaches the alveoli of the lungs, but is caught by the bronchial 
ciliated epithelium and in part coughed up, though part is car- 
ried into the submucous tissue, where some remains permanently 
and the remainder is conveyed by the lymphatics to the nearest 
glands, as peribronchial and even mediastinal glands and sub- 
pleural spaces. In rare cases the pigment reaches the general 
circulation and is deposited in the kidney, liver, spleen, and 
alimentary mucosa. 

Ingested pigments are likewise deposited in the alimentary 
mucosa and adjacent glands, or as in silver discoloration are dif- 
fusely distributed between the cells of the internal organs and 
tissues, and in the subepithelial layer of the skin, where de- 
posited in the form of silver albuminate, it is finally reduced, 
resulting in a bluish pigment. 



PATHOLOGIC PROCESSES 63 

In chronic lead poisoning, the bine line on the gums is due to 
the formation of lead sulphide. 

In tattooing, the pigments are found in the deep layers of the 
skin, and in the adjacent lymphatic glands. 

Hematogenous pigmentation may be (a) general or (b) local. 

(a) In the general form, blood is hemolyzed, liberating hem- 
oglobin into the blood stream (hemoglobinemia) ; as much of this 
as can be disposed of by the liver is converted into bile, while the 
remainder is excreted by the kidneys (hemoglobinuria) wholly 
or in part ; in the latter case some hemoglobin is broken up and 
deposited in various tissues. This is best seen in the liver (espe- 
cially in periphery of lobules), spleen and kidneys. 

(b) In the local form, as in thrombosis, and interstitial hemor- 
rhages (including bruises), blood escapes into the tissues, is in 
part eliminated and in part vailed off and and coagulated; the 
hemoglobin diffuses out and is broken up into the various deriva- 
tives of blood pigments in situ. The different shades of color from 
red or brown to black depend upon successive degrees of re- 
ductions of the pigments. 

Local pigmentation is seen in infarcts, hematomata, thrombi, 
extravasations, etc. 

A dark or black pigmentation, resembling melanin (''pseudo- 
melanin") is often seen in the abdominal region of dead bodies, 
due to sulphide of iron (ILS from gastrointestinal decomposition 
acting on the iron derived from the blood"). It may become more 
or less general in distribution, and also sometimes forms during 
life in and around gangrenous areas, and other localities where 
free or loosely bound iron and H 2 S come together. 

The greenish discoloration in the abdominal region of dead 
bodies is due to sulphur-hemoglobin, due to H 2 S plus undecom- 
posed hemoglobin. 

Hepatogenous pigmentation (jaundice) is found either in the 
tissues in solution or in crystal form (needles or rhombic plates) 
especially in liver, skin, mucous membrane, serous membrane and 
glandular and fatty tissues generally, less often in other tissues — 
the brain substance alone escaping. 

Malarial pigment is found in various tissues, especially in spleen, 
liver, kidney, bone marrow and brain. 

Metabolic pigments are found locally in certain tumors, as 



64 GENERAL PATHOLOGY 

melanotic sarcomata and carcinomata, pigmented moles, chloas- 
mic spots, etc., and generally in the skin in Addison's disease, 
cevere anemias and cachexias, abdominal tuberculosis, abdominal 
tumors, and senility. 

Lipochromes occur as stated under etiology, and parasitic pig- 
ments are found in the various tissues invaded by the organisms. 

Gross Anatomy. — Discoloration is seen as follows: 

In Lungs : 

(1) Dark or black in anthracosis (coal dust, smoke, etc.) as in coal miners. 

(2) Grayish in chalicosis (stone dust) as in stonecutters. 

(3) Brownish red in siderosis (iron dust) as in iron workers. 

(4) Grayish in calcicosis (lime dust) as in marble cutters. 

(5) Grayish in silicosis (silica dust) as in glass cutters. 

(6) Yellowish in aluminosis (clay) as in potters. 

(7) Rusty brown in tabacosis (tobacco dust), etc. 

In skin ; also gastrointestinal walls, kidney, liver, etc. 

Bluish color in argyria due to AgNO and other soluble salts and silver. 

Rarely other extraneous pigments cause discolorations, as in lungs. 
Hematogenous pigments if in sufficient amount Avill color the tissues: 

(1) Reddish brown when due to hemosiderin and hematoidin. 

(2) Dark or black when due to iron sulphide. 

(3) Dark or black when due to malarial pigment. 
Hepatogenous pigments : 

(1) Yellowish red, when due to bilirubin. 

(2) Yellowish green when due to bilivcrdin (oxidized bilirubin). 

Metabolic pigments appear (pathologically): 

(1) Dark brown or black in tumors, etc., due to melanin. 

(2) Yellowish brown in skin. 

(3) Yellow, brown or green in tumors, etc., due to lipochromes. 
Parasitic pigments are of various colors as 

blue in B. pyocyaneusj yellow in Actinomyces bovisj black in Mucor niger 
(on lingual papillae) ; brown in Microsporon furfur (tinea versicolor) ; etc. 

Pathologic Histology. — By transmitted light, extraneous pig- 
ments appear black, and usually coarsely granular and extra- 
cellular, though leucocytes are apt to contain them (phago- 
cytosis). 

Hemosiderin appears as intracellular (less often extracellular) 
fine irregular granules of yellowish or reddish brown color in 
various tissues, but is best seen in liver, spleen and lungs, fol- 
lowing congestion. A certain amount of oxygen seems to be 
necessary in its formation, therefore it is seen at the periphery 
of old necrotic areas, as blood clots, infarcts, etc. 



PATHOLOGIC PROCESSES 



65 




Fig. 11. — Anthracosis of the lung. (Delafield and Prudden.) 



66 GENERAL PATHOLOGY 

Hematoidin appears in fine acicnlar crystals or rhombic plates, 
or spherical grannies, usually a bright yellowish red, always be- 
tween cells and oftenest in the center of old blood clots or in- 
farcts. Oxygen must be absent when it is formed. 

Iron sulphide appears as black granules. 

Bilirubin, bilifuscin and biliverdin usually appear as fine 
granules, occasionally as crystals, yellowish to brown in color, 
intracellular, pigmenting the nucleus as well as the cytoplasm 
and are best seen in liver. 

Malarial pigment is a black, finely granulated pigment, found 
in the perivascular lymph spaces in organs and tissues, especially 
of the spleen, liver, kidney, and brain, also in the cells of these 
organs at times and in phagocytes. 

Melanin is seen as coarse granular, brownish black pigment 
in various tissues, as in melanosarcomata, usually within the 
cells though sometimes free in lymphatic spaces ; in marked cases 
it may appear in the blood (melanemia) and be excreted in the 
urine (melanuria) either as melanin, or as melanogen (colorless) 
which darkens (oxidizes) on standing. 

Lipochromes are seen within the cells of tumors, etc., and 
stain with the ordinary fat stains. 

Reactions. — Hemoglobin is composed of globin (protein) 96 
per cent and hematin 4 per cent. The latter contains the coloring 
matter of the blood. 

The two principal derivatives of hematin are hemosiderin 
(iron-containing) normally used for reconstructing hemoglobin, 
and hematoidin (iron free) isomeric with bilirubin, and nor- 
mally eliminated. 

Hemosiderin is colored blue (Prussian blue) when sections are 
treated with potassium ferrocyanide, 2 per cent aq. sol. followed 
by HC1 0.5 per cent in glycerin, or 1 per cent in alcohol (Perl's 
test). Hematoidin will not respond to Perl's test — since it con- 
tains no iron; hemoglobin will not, because its iron is too firmly 
united with the protein. 

Bile pigments give the Gmelin's reaction— a play of colors; 
viz., green, blue, violet, red and yellow, when adding a drop of 
commercial nitric acid. They also turn green with weak tincture 
of iodin. Hematoidin also responds to Gmelin's test. 



PATHOLOGIC PROCESSES 67 

Lipochromes are colored by Sudan in and Scharlach R, and 
usually by osmic acid. 

Extraneous pigments are usually insoluble; those soluble in 
acids evolve C0 2 . Carbon is distinguished from melanin and 
other dark pigments by its insolubility in strong H 2 S0 4 . 

Pathologic Physiology. — Large amounts of pigment may cause 
proliferation of connective tissues with atrophy of the paren- 
chyma, and consequent loss of function. 

Results. — Pneumonokoniosis is often followed by tuberculosis. 
Fibrosis follows nearly all forms of extraneous pigmentation. 

Internal pigments are apt to become absorbed in time, though 
in some cases they become encapsulated. 

Albinism is a deficiency or absence of normal amount of 
melanotic pigment. Leukoderma is an irregular distribution of 
pigment in the skin, some parts paler, others more pigmented. 
Canities is grayness or whiteness of hair, due to loss of color, 
probably resulting from decrease or loss of intracellular oxida- 
tion of the chromogen. 

Calcareous Infiltration 

Calcareous infiltration is the abnormal deposit of earthy salts 
in the tissues, chiefly phosphates and carbonates of calcium, 
though magnesium salts are also found. (Fig. 12.) 

Etiology. — Necrosed or diseased tissue seems necessary (with 
the possible exception of the calcareous metastases). The min- 
eral matter in solution is brought by the blood and lymph to 
the part, and by some local chemical process is deposited in in- 
soluble form. 

At present there is a tendency to consider that from the local 
disintegrated tissues, protein substances arise which unite with 
the calcium and magnesium, and subsequently are replaced by 
phosphoric and carbonic acids to form the corresponding salts; 
or that the fatty acids, liable to appear in degenerated areas, 
may form calcium and magnesium soaps and may likewise be re- 
placed by the stronger acids. 

Calcareous metastasis : In some rare cases of resorption of 
bone, as in extensive caries, osteomalacea, osteosarcoma, etc., 
there may be widespread deposition of salts in cartilage, lungs, 
gastric mucosa, arterial and capillary walls, etc. The tissue here 



68 



GENERAL PATHOLOGY 



is not known to have been previously diseased, though some 
claim that the deposit, being intercellular, is "in inert or dead 
tissue." Senile calcification of blood vessels, etc., has been 
classed as metastatic, since bone is absorbed in old age, but this 
depends probably upon the hyaline changes occurring in senile 
sclerosis. 

Locations. — Sclerotic vessel walls, especially, aorta, coronary, 
cerebral, radial, etc. 




Fig. 12. — Calcareous infiltration of the wall of a small artery from the wall of a gumma 
of the liver. Zeiss, Oc. 2; ob. D. D. (McFarland.) 



Endocardium (especially of valves); pericardium, myocardium, 
etc. 

Pituitary body; meninges; ventricular plexus; ganglion cells, etc. 

Necrotic foci, as tubercular, parasitic, etc. 

Sclerotic foci, as scars, infarcts, or thrombi. 

Joints. 

Tumors, especially the avascular, as fibroma (particularly 
uterine), and tumors involving bone and cartilage; also cysts, 
goiters, psammomata, etc. 

Long retained dead fetuses (litliopodia). 



PATHOLOGIC PROCESSES 69 

Concretions within the organs or their ducts, as tonsils, pros- 
tate, etc. 

Gross Morbid Anatomy. — When the deposit is abundant, the 
parts are hard and brittle, of white, gray, or yellow color and 
opaque appearance. The lesions are gritty to the touch and 
section knife. Old tuberculous calcified areas are apt to be sur- 
rounded by pigmented fibrous tissues, especially in lungs and 
bronchial glands. 

Pathologic Histology. — Fine intercellular granules, less often 
intracellular (as in the ganglion cells) are seen, appearing black 
by transmitted, and white and glistening by reflected light, By 
coalescence, larger masses form, usually with concentric layers. 
In blood vessels, serous membrane, etc., calcareous plates are 
seen. When intracellular, the cells show degeneration. 

Reactions. — Acids will dissolve the granules, and in case of 
carbonates with evolution of gas (C0 2 ), observable under the mi- 
croscope by running 5 per cent HC1 solution under cover-slip. 
To differentiate between lime and other salts soluble in HC1, 
add concentrated H 2 S0 4 , which forms needles of CaS0 4 (gyp- 
sum). Lime salts stain blue with hemotoxylin. and black with 
AgN0 3 . 

Pathologic Physiology. — Function is impaired or destroyed by 
pressure, or inflammatory conditions are caused by irritation. 
In calcified blood vessels, nutrition to various tissues is re- 
stricted. 

Results. — Very small deposits may be absorbed, but usually 
there is proliferation of connective tissue, with capsule forma- 
tion. Sometimes degeneration of adjacent tissues is caused by 
the calcareous masses. 

Ossification. — Ossification which is the deposition of lime salts 
in a uniform regular order, as in normal bone formation, by the 
activity of certain cells (osteoblasts) occurs pathologically in 
tumors connected with cartilage, bone, and periosteum, and in 
ossifying inflammation of muscles (myositis ossificans). 

Concretions or Concrements 

While calcareous infiltration is a deposit within tissues, con- 
cretions are deposits of lime and other substances within the 
ducts and cavities of the body. 






70 GENERAL. PATHOLOGY 

In the formation of concretions there is always a small mass 
of mucus, desquamated epithelium, secretory matter, parasites 
or foreign bodies; in other words, usually some pathologic prod- 
uct upon which, as a nucleus, the various salts or substances 
forming the bulk of the concretion are deposited, "much as cane 
sugar crystallizes on a string to form rock candy, but with the 
important exception that the concretions are mixed with mucin 
or other organic matter which remains as a frame work when 
the salts are dissolved out." 

Gallstones (biliary calculi) are made up of variable amounts 
of cholesterin, the chief constituent of the great majority of 
these stones, and of bile pigments and calcium. Renal calculi 
(kidney stones) are composed of uric acid, oxalate of lime, or 
phosphates; less frequently of other substances. Vesical cal- 
culi (of the urinary bladder) are composed of phosphates, uric 
acid, and oxalates of lime ; rarely of other substances. 

Calcium salts form the chief mineral constituent of rhinoliths, 
broncholiths, phleboliths (which are calcification of organized 
thrombi; often found in the prostate or uterus), salivary, ton- 
sillar, lacrimal, cutaneous, appendicular, pancreatic and preputial 
concretions and prostatic calculi. In the intestines, concretions 
or enteroliths, usually consist of ammonio-magnesium phosphates, 
though the finer "intestinal sand" consists of calcium. Occa- 
sionally concretions of fat and soaps may follow the ingestion 
of large doses of olive oil, and be mistaken for gallstones. 

Hydropic, Dropsical, or Serous Infiltration 

Hydropic infiltration is an excess of fluid within the cells in 
the form of globules. It must be distinguished from edema, 
dropsy, or anasarca, which is due to an outpouring of serum from 
the blood vessels into the tissues to an abnormal degree, while 
in hydropic infiltration certain cells imbibe more fluid than nor- 
mal, though the lymph surrounding them may not be abnormal in 
quantity. (Fig. 13.) 

Etiology. — The etiology is not definitely known, apart from 
a disturbed osmotic pressure, which may be due to "dissociation 
of the colloids, whereby crystalloids are liberated into the cyto- 
plasm" causing endosmosis of lymph. Toxins are probably a 
causal factor, at least in some cases (smallpox). 



PATHOLOGIC PROCESSES 71 

Gross Morbid Anatomy. — If abundant, the part is enlarged, 
soft, and boggy. 

Pathologic Histology. — Vacuoles of varying sizes, containing 
serous fluid, are seen in the cells, which are enlarged and in some 
cases ruptured. 

In edema the cells also may contain fluid, i.e., edema may be 
accompanied by hydropic infiltration. 

Locations. — Any type of cells may be affected, but most com- 
monly the epithelial cells, as those of mucous membranes, glan- 
dular viscera, epithelial tumors, etc. 

Results.— This condition is not serious, unless very extensive. 




Fig. 13. — Dropsical infiltration of the epithelial cells of a carcinoma of the breast: a, 
ordinary epithelial cells; b, b, dropsical cells; c, dropsical nuclei; d, enlarged nucleoli. 
(Ziegler.) 

Glycogenic or Glycogenous Infiltration 

Glycogenic infiltration is an infiltration of glycogen in cells 
normally free from it, or an excessive deposit in cells which 
normally contain it. 

Etiology. — The cause of pathologic deposits is not known. 

Locations. — In diabetes (in which disease it is most frequently 
found) glycogen occurs in the renal epithelium, heart muscle, 
liver, and leucocytes. In tumors, it occurs within the tumor cells, 
especially those of malignant connective tissue tumors. In septic 
and inflammatory conditions, the local cells and leucocytes are 
affected. Glycogen granules may also be found free in the blood 
stream. 

Gross Morbid Anatomy. — Sometimes an organ is slightly en- 
larged; often there is no change. 






7Z GENERAL PATHOLOGY 

Pathologic Histology. — Small globules or granules are seen usu- 
ally within the cells, but sometimes also between the cells, or 
even free in the blood or in fluid exudates. The intracellular 
granules are usually near the nuclei, which are usually well pre- 
served, even in advanced cases. 

Reactions. — Soluble in water, the granules are dissolved and 
leave empty spaces when sections are treated with water; the 
margins of these spaces for some unknown reason tend to take 
the basic stains. To preserve the glycogen in the tissues, the 
latter must be fixed in alcohol (in which glycogen is insoluble) 
and rapidly — because the granules quickly change into glucose 
after death of the tissue. 

Glycogen stains mahogany brown (as does amyloid) or wine 
color with iodine dissolved in glycerin, or in the form of the 
tincture diluted with four parts of absolute alcohol. No blue 
color is produced on adding H 2 S0 4 . The brown color disappears 
on heating, or on addition of alkalies, but reappears respectively 
on cooling or acidifying. 

Ptyalin rapidly converts glycogen into dextrose, and may be 
used on a section, showing microscopically whether the granules 
are grycogen. 

Pathologic Physiology. — Normally glycogen is formed within 
the cells by intracellular enzymes, which dehydrate and poly- 
merize the sugar brought by the blood. The liver and the mus- 
cles are the chief normal storehouses of glycogen, which when 
needed by the tissues is again converted into dextrose by a re- 
verse enzymotic process. Pathologically, glycogen is diminished 
or absent from the normal situations, and appears in excess in 
other locations. 

The result is always serious, since the accompanying or causal 
conditions, as diabetes, malignant tumor, etc., are usually fatal. 

Necrosis 

Necrosis means death of tissue. There are three grades: 
1. Necrobiosis, or death of individual cells, occurring path- 
ologically in the various degenerations, and normally in the break- 
ing down of secreting cells, as in the formation of sebum, and 
in other cells, conspicuously the outer cells of the epidermis. 



PATHOLOGIC PROCESSES 73 

2. Necrosis proper, or death of a portion of a tissue in the 
midst of, or attached to, living tissue. 

3. Somatic death — death of the entire organism. 

Necrosis — by which term the second form is usually referred 
to — has the following general etiology: 

1. External agencies, as heat, cold, electricity, x-ray, trauma, 
poisons, microorganisms. 

2. Internal agencies, as circulatory and nutritional disturb- 
ances, trophic and vasomotor influences, toxins. 

These various causes do not always produce the same type of 
necrosis, but may cause one form in some cases, and another in 
other cases. Any part of the bod}' may be affected. When in- 
volving soft tissues, about to be detached, the area is called a 
sphacelus, or slough; when involving a bone, a sequestrum. 

Changes may be seen in the intercellular substances and cells; 
the latter become shrunken or swollen, fragmented or dissolved 
(cytolysis) and take the stain very poorly. The nuclei may show 
fragmentation of the chromatin (karyorrhexis) with extrusion of 
the fragments into the cytoplasm where they finally disappear; 
or may retain their form but stain less and less distinctly until 
they dissolve (karyolysis) ; or may shrink (pyknosis) staining 
more deeply, before they dissolve and disappear. 

Fate of Necrotic Tissue: 

1. It may be absorbed, with regeneration of normal tissue, or 
with scar formation. 

2. It may be retained, and become encapsulated. 

3. It may be removed en masse spontaneously or artificially. 

The following types are usually recognized : 

Coagulation necrosis. 

Liquefaction, or colliquative, necrosis. 

Caseous necrosis, or caseation. 

Fat necrosis. 

Gangrene. 

Coagulation Necrosis 
Coagulation necrosis is death of tissue in which the protein 
suffers a change similar to, or identical with, coagulation (Fig. 14). 
Coagulation is the conversion of the soluble colloids into an 
insoluble form. 



74 GENERAL PATHOLOGY 

Etiology. — Any of the general causes already mentioned, but 
especially physical agents, as heat, cold, and trauma. Loss of 
nutrition, as in infarcts. Chemicals, as caustics. Toxins, espe- 
cially of pyogenic cocci, B. tuberculosis, and B. diphtherise. 

Physical and chemical agents cause coagulation by direct ac- 
tion. In exudates the action is analogous to, or identical with, 
blood coagulation, which consists of the conversion of fibrinogen 
(present in blood, lymph and exudates) into fibrin by action of 
the thrombin (fibrin ferment). The thrombin is thought to be 
produced when "prothrombin" (possibly a nucleo-protein ex- 
isting in leucocytes, blood platelets and tissue cells, and liberated 
when these are injured) is activated by the calcium salts of the 
blood or lymph. 




Fig. 14. — Coagulation necrosis of the hepatic cells in a case of puerperal eclampsia. 

(Karl and Schmorl.) 

In anemic areas the tissue cells possibly coagulate from the 
action of coagulins contained within the cells, though this has 
never been actually demonstrated. When lymph infiltrates such 
areas, fibrin is formed. 

Locations. — Seen in tissues rich in protein, especially. 

1. In bloodless parts, as anemic infarcts, and tubercles in the 
early stages of tuberculosis. 

2. In inflammatory exudates, including "false membranes" 
upon mucous surfaces, fibrinous exudates upon serous surfaces, 
around abscesses and ulcers. 

3. In blood clots — extravascular or intravascular (thrombi), in 
interstitial hemorrhages and hemorrhagic infarcts. 






PATHOLOGIC PROCESSES 75 

4. In striated muscles, in cases of typhoid and other fevers. 

Gross Pathology. — The parts are usually dry, firm, pale, glazed 
and more or less swollen. Solid tissues present the appearance 
of boiled flesh. Later the color becomes grayish and the part 
inclines to soften. False membranes, which are a coagulation 
necrosis of certain inflammatory exudates, have a gelatinous or 
mucoid consistence, and are not readily detached from the un- 
derlying tissue. 

Blood clots are red and semifluid, and break with a gelatinous 
fracture when fresh ("currant jelly" clots) ; are yellow and 
gelatinous when leucocytes predominate ("chicken-fat" clots) ; 
and "white" clots when the cells have largely disappeared and 
fibrin alone remains. 

Pathologic Histology. — The cells lose their staining power 
early, become indistinct, and later disintegrate completely. Mus- 
cle cells lose their stria 3 , and in cardiac muscle the intercellular 
cement substance often dissolves out, and the fibers separate and 
may present vacuolation and fragmentation. The nuclei stain 
faintly and later disappear. 

The blood vessels at the margins of the necrosed area are 
thrombosed. In blood clots, there is usually more or less fibrin, 
which in recent clots consists of a dense reticulum of fine fibril- 
he with "nodal points" at their points of intersection. In older 
clots and in exudates the nodal points are not seen, the fibrils 
are less distinct, or the fibrin may appear as granules. In anemic 
infarcts or other anemic areas, the fibrin is very small in amount 
or may be wholly absent, and in any case may require special 
staining (as Weigert's) to demonstrate. 

Physiologic function is usually considerably disturbed. 

Results. — Small areas may be liquefied and absorbed. Larger 
areas may undergo caseation and calcification, or may liquefy 
and suppurate and be replaced by normal tissue or by scar tis- 
sue ; they may also liquefy and become encysted. 

Liquefaction Necrosis 

Liquefaction necrosis is death of a tissue with transformation 
into fluid. It may be primary, as in the central nervous system; 
or secondary, as when following coagulation necrosis, cheesy 
necrosis, inflammation, gangrene, and tumors. 



76 GENERAL PATHOLOGY 

Etiology. — 1. Lysins, or liquefying enzymes are the causal fac- 
tors. Aseptic softening following proteolysis by enzymes either 
from the dead cells (autolysis) or from leucocytes (heterolysis). 
In septic softening, the bacteria elaborate the lysins, as in sup- 
puration, gangrene, etc. 

In the central nervous system, thrombosis of a terminal artery 
(infarcts) which elsewhere would cause coagulation necrosis, here 
causes liquefaction necrosis — cause being unknown, probably lack 
of coagulins. 

2. Fluids may infiltrate the tissues and dissolve them. 

Locations. — Liquefaction necrosis occurs in any tissue. It is 
common in acute inflammation, abscesses, vesicle or cyst forma- 
tion, and in anemic and hemorrhagic infarcts of brain. 

Gross Pathology. — The tissue is soft, at first semifluid, pale or 
yellow from fatty material, reddish brown or greenish from blood 
pigments or bile. Later there is fluid containing broken down 
cells and debris. 

Microscopically. — The cells undergo disintegration, fat, choles- 
terin, etc., being liberated, resulting in a fluid debris, containing 
granules, and a few leucocytes which are sometimes engorged 
with fat globules. 

Results. — The contents may coagulate, become encysted, be 
absorbed or discharged, and the space if small, occupied by nor- 
mal tissue, or if larger, by connective tissue (cicatrization). 

Cheesy Necrosis, or Caseation 

Cheesy necrosis, or caseation is death of a part with the forma- 
tion of a cheese-like material. (Fig. 15.) 

Etiology. — Toxins, especially of B. tuberculosis. It may fol- 
low coagulation, or as some state it, be a form of coagulation 
necrosis of the proteins with appearance of a certain amount 
of fat, 

Locations. — Old tuberculous lesions, gummata, blood clots, in- 
farcts, and areas of coagulated necrosis. The typical cheesy 
necrosis is that occurring in tuberculosis; whether that which 
occurs in other situations is true caseation is still a disputed point. 

Gross Pathology. — The area is pale yellow with the appearance 
of cheese, but more granular. A dry form occurs which is rounded, 



PATHOLOGIC PROCESSES 



77 



circumscribed, and often encapsulated, and never larger than a 
hazelnut. 

The moist form is softer, paler, and less sharply circumscribed. 

Microscopically. — Fine granules of protein material, with fatty 
debris, are seen, the latter in advanced cases showing fatty acid 
and cholesterin crystals, and sometimes leucin and tyrosin. The 
cells can not be recognized, at least in fully developed cases, 
except some of the leucocytes. 

Results. — Areas may persist a long time without undergoing 
change or absorption (possibly due to destruction of autolysis by 







Fig. 15. — Large tubercle of the lung, showing cheesy necrosis. (Stengel and Fox.) 

toxins); the leucocytes do not enter the area (lack of chemotac- 
tic substances). 

Finally calcification occurs, or cysts form which may persist, 
or be absorbed with cicatrization. 



Fat Necrosis 

Fat necrosis is a form of necrosis occurring in fatty tissues 
and apparently due to the action of pancreatic juice. 

Etiology. — It is believed that trypsin injures the cells, and 
the lipase (steapsin) splits the fat into fatty acids and glycerin, 
the latter being absorbed (and may appear in the urine) while 
the acids later unite with calcium to form insoluble soaps. 



78 



GENERAL PATHOLOGY 



Any condition permitting escape of pancreatic juice from its 
normal channels, as obstruction of the duct, acute pancreatitis, 
tumors, etc., may act as a cause. 

Locations. — This necrosis is seen in abdominal walls, the fat in 
and around the pancreas, etc. 

Gross Pathology. — The areas are white or yellowish, circum- 
scribed, varying from the size of a pinhead to a pea, may be soft 

















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Fig. 16. — Focal necrosis in the liver in pneumonia. (Delafield and Prudden.) 

or gritty, and may or may not be surrounded by an inflammatory 
border. 

Microscopically. — Usually but little of the original structure 
remains. The necrotic debris consists chiefly of calcium soaps, 
crystals of fatty acids, etc. 

Results. — While the necrotic areas themselves are not danger- 
ous to life, the causal conditions are usually fatal. When re- 
covery does take place, the necrotic foci disappear quickly. 

Focal Necrosis 

Small areas of necrosis (microscopic in size or sometimes visi- 
ble to naked eye) are often found in the liver, less often in the 



PATHOLOGIC PROCESSES 79 

kidney, spleen and elsewhere, in eases of typhoid fever, less often 
diphtheria, septicemia and other infections, and presumably due 
to toxins. (Fig. 16.) 

Gangrene 

Gangrene has been defined as (1) death of a considerable mass 
of tissue, which may become dried (dry gangrene, or mummifica- 
tion) or may putrefy (moist gangrene) due to saprophytic inva- 
sion, or (2) and probably more correctly, as putrefaction of ne- 
crotic areas. 

Primary gangrene is that due directly to bacterial invasion, as 
in malignant edema, and hospital gangrene. 

Secondary gangrene is necrosis subsequently invaded by bac- 
teria. 

Etiology. — The various causes as given under necrosis apply 
here. Putrefactive bacteria are said to be present in all cases, 
but as the fluid evaporates from the part, as in superficial tissues, 
bacterial action becomes less and less conspicuous, and finally, 
in complete mummification, ceases. 

Dry gangrene is oftenest caused by arterial obstruction ; freez- 
ing may block the vessels with thrombi; ergotism and Raynaud's 
disease may contract the vessels and shut off the blood supply; 
senile gangrene is due to arteriosclerosis with enfeebled heart 
action. Dry gangrene may also follow moist gangrene when 
putrefaction is slow and evaporation marked. (Fig. 17.) 

Moist gangrene is usually due to venous obstruction, but may 
follow any circulatory obstruction or destructive agency: (a) 
Strangulation of a part — bowel, appendix, torsion of spleen, kid- 
ney, tumor, etc. (b) Internal emboli as in pulmonary arteries 
and veins, or mesenteric arteries, (c) In the lungs, it may fol- 
low pneumonia, abscess, bronchiectasis, tumors, and diabetes. 
(d) In extremities, it may follow trauma, diabetes, physical 
agencies, etc. (e) In mucous membranes, it may follow the ac- 
tion of toxins, as in noma of the mouth or genitals, (f) In 
cystitis, it may follow trophic disturbances, (g) In decubitus, it 
is due to trophic and circulatory disturbances combined. 

Locations. — Any part may be affected, but particularly the 
distal ends of upper and loAver limbs, bowels, lungs, etc. 



80 



GENERAL PATHOLOGY 



Gross Pathology. — Gangrene is a dark greenish or black (some- 
times "white" or anemic, especially in early stages) area, tem- 
perature is below normal, the area is usually circumscribed, and 
more or less odorous. The part is separated from the living tis- 




Fig. 17. — Senile dry gangrene of the lower extremity, showing line of demarcation. 

(Hektoen.) 

sue by a red inflammatory narrow zone — "the line of demarca- 
tion." 

The dry form has the folloAving distinctive features: The part 
is harder and the surface rough, shrunken, noncrepitant, of slight 
odor, and nearly always circumscribed. The line of demarcation 
advances slowly. 

The moist form has the following distinctive features: Is 
softer than normal, somewhat swollen, skin covered with vesicles 



PATHOLOGIC PROCESSES 81 

or blebs, and discolored fluids ooze from sections or injured parts. 
There is crepitation, due to gases of decomposition. The line 
of demarcation advances more rapidly than in the dry form. 
Occasionally there is no line of demarcation, as in diabetes. Oc- 
casionally there are metastatic forms of gangrene. 

Pathologic Histology. — The cells have become converted into 
granular debris, consisting of protein matter, fatty granules, 
crystals of fatty acids, cholesterin, leucin, tyrosin, phosphates, 
carbonates, blood pigments, etc. The connective tissue and elas- 
tic fibers persist longer than the cells, but finally become lique- 
fied. Bacteria are also present. 

Results. — The process may go on until by absorption of toxic 
products death ensues (especially true of the moist form, due 
to primary invasion of bacteria, or to disease as diabetes). In 
other cases the mass is cast off as a slough or sphacelus at the 
line of demarcation, or encysted if within the body, followed 
by resorption and calcification or cicatrization of the gangrenous 
materials. 



CHAPTER IV 

THE CIRCULATORY CHANGES 

The circulatory changes are usually studied under the follow- 
ing headings: (a) Ischemia, or Local Anemia; (b) Hyperemia; 
(e) Hemorrhage; (d) Thrombosis; (e) Embolism; (f) lufarcts; 
and (g) Edema. 

Ischemia, or Local Anemia 

Ischemia, or local anemia, is a decrease of blood in, or total 
absence from, some part of the body. 
Etiology. — According to cause we have — 

1. Collateral anemia, due to blood having passed in excess to 
some other part, as cerebral anemia from shock or fainting, the 
blood passing to the dilated abdominal vessels. 

2. Obstructive anemia, or ischemia, due to obstruction of the 
blood supply to any part, as anemic infarct, pressure of tumors, 
tight bandage, ligatures, cicatrices, obliterating endarteritis, 
etc. 

3. Neurotic anemia, due to (a) stimulation of the vasoconstric- 
tors (neurotonic anemia) as in the first stage of Raynaud's dis- 
ease, ergotism, etc., or to (b) paralysis of the vasodilators (neu- 
roparalytic anemia) as in pallor from strong emotions, fright, 
anger, etc. 

4. Anemias due to causes acting directly on the vessels and 
in other ways not fully understood (hence the "idiopathic ane- 
mias" of some authors), as heat, cold, toxins, etc. 

Gross Morbid Anatomy. — The part is pale, lower in tempera- 
ture, smaller in size, less in weight, and more or less bloodless 
on section. 

Minute Anatomy. — Blood cells are abnormally decreased or ab- 
sent from the vessels. In long standing cases, atrophy, degenera- 
tive and necrotic changes may be noted. 

Pathologic Physiology. — Function is unaffected or may be di- 
minished. Occasionally the part is painful or tremulous. 

82 



CIRCULATORY CHANGES 83 

Results. — Mild degrees recover, especially if treated. In cases 
due to blocking of the vessel, anastomotic circulation may fully 
restore the part. In severe and prolonged cases, atrophy, de- 
generative and necrotic changes result. 



Hyperemia 

Hyperemia is excess of blood in a part. It is active when 
excess of blood is brought to a part by the arterial system; pas- 
sive, when the normal removal of blood is interfered with by 
the venous system. 

Active Hyperemia 

Etiology. — According to cause we have — 

1. Collateral hyperemia, due to anemia in another part, as 
around anemic areas, or by bandaging a limb preparatory to 
amputation, etc. 

2. Increased heart action may cause hyperemia, though proba- 
bly only supplementary to other causes or local conditions. 

3. Neurotic hyperemia, due to (a) stimulation of vasodilators 
(neurotonic hyperemia) as in certain forms of neuritis, as herpes 
zoster, or the rash of teething infants, etc., also in erythro- 
melalgia (red, painful, pulsating areas of hands and feet) blushing, 
etc., or due to (b) paralysis of vasoconstrictors (neuroparalytic 
hyperemia) as in hyperemia of a side of the face from pressure 
of a tumor upon the cervical sympathetic; certain forms of 
migraine may also belong here. 

4. Cases due to agencies whose action is imperfectly under- 
stood, as heat, reaction from temporary pressure, certain drugs, 
toxins, increased functional demand, etc. 

Gross Anatomy. — The part is red — color disappearing on pres- 
sure, temperature of superficial parts somewhat raised, size and 
weight increased (due in part to hypertrophy). The part is 
bloody on section. 

Minute Anatomy.— The vessels are abnormally filled with blood, 
occasionally there is a capillary hemorrhage into the tissues. 

Pathologic Physiology. — Function is unaffected or increased 
when hyperemia is moderate and uncomplicated. In tensely 
filled encapsulated organs the function may be impaired from 
compression of the parenchyma. 



84 GENERAL PATHOLOGY 

Results. — Mild cases recover. Mild prolonged cases may cause 
hypertrophy. In severe and prolonged cases capillary hemor- 
rhage may occur, or the vessels may remain weak and liable 
to repeated dilatation from slight causes or be followed by in- 
flammation. 

Passive Hyperemia 

Etiology. — 1 General causes are enfeebled heart action from 
obstructive heart disease or from any cause ; also insufficient 
muscular exercise, disease of lungs interfering with outflow of 
blood from right side of heart, etc. 

2. Local causes, as pressure on veins by tumors, aneurysm, 

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Fig. 18. — Chronic passive congestion of the liver. (Delafield and Prudden.) 

etc., or interference of passage of blood through veins as parietal 
thrombi, syphilitic or other phlebitis, etc. 

Gross Anatomy. — The part or organ affected is dark or bluish 
(cyanotic), the color disappearing on pressure. The brain and 
cord, however, are not cyanotic when congested. Size and 
weight are increased, temperature of superficial parts reduced. 
(Fig. 18.) 

Minute Anatomy. — All vessels are distended with blood. 
Edema (excessive lymph within tissues) is often noted. In 
prolonged cases, other forms of degenerations may be seen. 

Pathologic Physiology. — Function is impaired. The part or 
organ is at first painful, later anesthetic (probably pressure on 
nerve endings). 



CIRCULATORY CHANGES 85 

Results. — Mild cases may recover, but the process is more apt 
to be chronic than in the active hyperemia. Gradually developed 
and prolonged cases lead to atrophy, degeneration, edema, pig- 
mentation or cyanotic induration (fibrosis). Severe and rapidly 
developed cases may lead to coagulation necrosis and gangrene. 

Hypostatic Congestion 

Hypostatic congestion is passive congestion or hyperemia oc- 
curring in dependent parts, due to enfeebled heart action. It 
occurs especially in debilitating diseases, in low fevers, and also 
commonly just prior to death from any cause, and is seen usually 
in the skin and subcutaneous tissues of back and buttocks, and 
in the lungs. 

Hemorrhage 

Hemorrhage is the escape of blood from blood vessels. 
Type I. According to source of blood: 

(1) Arterial hemorrhage. (2) Venous. (3) Capillary. (4; 
Mixed, or parenchymatous. 
Type II. According to mode of production : 

(1) Hemorrhage by rhcxis or laceration. 

(2) Hemorrhage by diabrosis or ulceration, caustic action. 

(3) Hemorrhage by diapedesis or oozing of blood from capil- 

laries or venules through the intercellular cement spaces 
("stomata") and due to increased blood pressure or 
altered vessel walls. 
Type III. According to destination: 

(1) External Hemorrhages — upon exterior of body or into cavi- 

ties communicating therewith, as 
Epistaxis — hemorrhage from nose 
Hemoptysis " " lungs. 

Hematomesis " " stomach. 

Hematuria tl " urinary tract. 

Enterorrhagia " " intestines. 

Metrorrhagia " " uterus between menses. 

Menorrhagia " " uterus during menses. 

Hematidrosis " " sweat glands. 

(2) Internal Hemorrhages into 
(a) Closed cavities, as 

Hemothorax — hemorrhage into pleural cavity. 
Hemoperitoneum " into peritoneal cavity. 

Hemopericardium ' ' into into pericardial sac. 

Hematocele " into tunica vaginalis testis 

or other small cavity. 



86 GENERAL PATHOLOGY 

(b) Interstitial or Concealed Hemorrhages, as 

EcchymOsis — circumscribed hemorrhage beneath skin or 

mucous membrane. 
Suffusion of Blood or Suggillation — diffuse hemorrhage 

in same locations. 
Petechias — minute or circumscribed hemorrhage (often 

punctif orm) . 
Hematoma — a tumor-like collection of blood. 
Hemorrhagic Infarct — a wedge shaped area of blood. 

Etiology. — (1) Traumatism. (2) Erosion by surrounding dis- 
ease, as ulcer, tuberculous cavity, etc., or by corrosion of caus- 
tics. (3) Increased blood pressure, as in great excitement, mus- 
cular effort, increased atmospheric pressure (caisson disease), 
hypertrophied heart associated with arteriosclerosis, etc. (-4) 
Alteration of vessel walls, resulting from degenerative changes, 
as in aneurysm, apoplexy, cachexia 3 , pressure atrophy, poisons, 
toxins of bacteria, plants or snakes. (5) Nervous influences: 
disease or section of the cord, apoplexy, suppression of men- 
struation, etc., sometimes cause hemorrhage from other parts, as 
stomach, nose, etc. 

Gross Anatomy. — The blood may be bright red. dark or black, 
according to length of time retained in tissues or cavity. In in- 
terstitial hemorrhage the part is swollen. 

Microscopically, the tissue is infiltrated with blood cells or 
blood pigment, and where coagulation has occurred, fibrin may be 
seen. 

Hemorrhage is checked by: (1) Formation of clot plugging 
the bleeding vessel. In certain conditions, especially hemophilia 
(see below) the blood shows little or no tendency to clot. (2) 
Reduction of blood pressure. (3) Contraction of vessel at site 
of hemorrhage with retraction and curling up of the middle coat 
in cases in which arteries are cut transversely. The contraction 
is usually followed in a few hours by relaxation, which may 
cause secondary hemorrhage. (4) Pressure of extravasated blood 
upon capillaries in interstitial hemorrhages. 

Results. — Depending upon age, health, etc., about Y 5 to Vi 
of total amount of blood in body may be lost without fatal re- 
sults. One large hemorrhage is more apt to result seriously than 
a larger amount of blood lost in small and oft repeated hemor- 
rhage. The total amount of blood (usually given as % 3 ) is 



CIRCULATORY CHANGES 87 

probably only % 6 to y 20 of the body weight, or about 8 pounds 
for average adult. 

Blood escaping into a large smooth cavity (as pleural or peri- 
toneal) does not clot readily and may be wholly or in large part 
absorbed by lymphatics and returned to the circulation. 

Hemophilia 

Hemophilia is a condition characterized by spontaneous or 
readily induced homorrhages, and especially by delay or absence 
in clot formation at the site of hemorrhage. 

It is usually hereditary though acquired cases are also re- 
ported. Males are much more frequently affected than females 
(about 12 to 1), but the diathesis is almost exclusively transmit- 
ted through the female sex. 

Pathology. — Various alterations in the blood have been ob- 
served, as a deficiency in calcium salts, in blood platelets and in 
prothrombin but these changes are not constant. The shed blood 
in many cases coagulates as rapidly and as firmly as in normal 
conditions. The occurrence of local hemophilia (where vessels 
in certain regions alone show this tendency) argues against gen- 
eral blood changes. It is probable that the prothrombin neces- 
sary for fibrin formation at site of hemorrhage is largely fur- 
nished by the endothelial cells of the vessel walls, and the theory 
has been advanced (Sahli) that these cells are deficient in this 
particular enzyme in cases of hemophilia. 

Results.— Hemophiliacs or "bleeders" are apt to succumb to 
fatal hemorrhage during the early years of life — the later the 
diathesis manifests itself, the more favorable the prognosis. 
Secondary anemia is usually observed. 

Thrombosis 

Thrombosis is coagulation of blood in heart or blood vessels 
during life. The coagulum is called a thrombus. Occasionally 
thrombi of fibrin and leucocytes appear in the lymph vessels. 

Coagula formed postmortem, or those formed outside of the 
vessels are called clots, (this distinction is, however, not main- 
tained by all writers). 

Types of thrombi: 



S8 . GENERAL PATHOLOGY 

I. According to extent and time of formation: (1) Primary 
thrombi are those first formed and confined to the original site. 
(2) Propagated thrombi — those portions subsequently formed and 
reaching to the nearest branch of the vessel or further (some call 
these "secondary"). (3) Secondary thrombi — those formed upon 
an embolus detached from a primary thrombus, or upon a pre- 
existing thrombus. 

II. According to location: (1) Cardiac; arterial; venous, in- 
cluding portal; capillary; and lymphatic. (2) Proximal — those on 
the cardiac side of a causal obstruction; and distal — those on the 
other side of the obstruction. 

III. According to shape: Parietal; annular; valvular; ob- 
literative; saddle or riding (at bifurcation of vessels) ; polypoid 
or pedunculated, seen usually in left auricle ; ball thrombi — de- 
tached pedunculated forms. 

IV. According to composition: (1) Red or currant jelly thrombi 
— rapidly formed, as in complete stasis, ligation, and death (post- 
mortem clots), and containing all the cellular elements of the 
blood. (2) Yellow or chicken-fat thrombi — slowly formed, as in 
prostrating diseases, or in slowly approaching death, the red 
cells gravitating to the lower parts, leaving the white cells on 
top. The chicken-fat clot is formed after death in anemic, espe- 
cially leucemic diseases. (3) White thrombi — consist of fibrin with 
a varying number of leucoc} T tes and of platelets; are formed in 
flowing blood, and occur in heart and large vessels, as peduncu- 
lated or parietal forms. (4) Stratified thrombi — consist of alter- 
nating laminae of white and red cells, due to alternating slowing 
and accelerating of the blood current, and seen in dilated vessels 
and aneurysms. (5) Marantic, thrombi are dark colored, composed 
almost wholly of red cells, seen in dependent vessels, in brain 
sinuses, etc., and in the lower parts of chicken-fat thrombi; they 
are due to enfeebled circulation and exhaustive diseases, maras- 
mus, etc. Many of these thrombi have been found to be in- 
fective. (6) Agglutinative or hyaline thrombi appear to be 
homogeneous and colorless; usually seen in plaque thrombi, which 
are composed of blood platelets fused together, and occurring usu- 
ally in the heart and large vessels ; also in conglutinative thrombi, 
consisting of almost colorless red blood corpuscles fused together 
and seen in diseases attended with hemolysis; as anemias, infec- 



CIRCULATORY CHANGES 89 

tions, poisons, etc. These occur usually in small visceral veins. 
(7) Organized thrombi — those which have been replaced wholly or 
in part by new connective tissue. (8) Calcified thrombi — found 
usually in veins, as phleboliths, and rarely in arteries as arte- 
rioliths, and in heart as cardioliths. (9) Canalized thrombi — those 
through which an opening has been formed by simple softening 
(liquefaction necrosis) or rarely by dilatation of a longitudinally 
disposed newly-formed blood vessel in an organized thrombus. (10) 
Infective thrombi — may be infective from the start, as in septic 
emboli, or may be subsequently infected. 

Etiology. — (1) Altered cardiac or vessel walls. Any agency 
which roughens the intima or endocardium, as injury in ligation 
or laceration, pressure of tumors, etc., or disease as atheroma, 
local inflammatory or degenerative conditions, or action of para- 
sites, tissue cells, etc. (2) Altered rate of blood current. Slow- 
ing favors agglutination of leucocytes and platelets to cardiac 
and vessel walls and to one another. Thrombosis is apt to occur 
in sinuses of the heart, and brain ; in dilated vessels, aneurysms, 
etc. (3) Emboli. (4) Altered blood. Experimentally the in- 
jection of tissue extracts (thymus, suprarenal s, etc.) containing 
fibrin ferment; of hemolytic agents, as nitrobenzol, ether, phenol, 
phytotoxins, zootoxins, and bacterial toxins will cause thrombosis. 
Increase of calcium salts, hyperinosis as in pregnancy, etc., favor 
thrombosis. 

Gross Anatomy. — Fresh thrombi are jelly-like, moist and break 
with a gelatinous fracture. Old thrombi are firm, due to fibrosis 
or calcification. The color depends upon the type. 

The postmortem clot is distinguished from a thrombus by be- 
ing loose, showing no evidence of attachment to heart or vessel; 
is moist and shows no distinct stratification, though in slowly 
forming clots, the upper layer may be paler than the lower. 

Microscopically. — Freshly formed fibrin presents a dense net- 
work of very fine fibrils, with "nodal points" or granular mat- 
ter at the points of intersection. The blood cells are usually 
present in normal proportion. In older thrombi, red and white 
cells or fibrin predominate, as stated under the various types. 
In organized thrombi, young connective-tissue cells and fibers, 
and newly formed capillaries are seen, the elements of the thrombi 



90 GENERAL PATHOLOGY 

disappearing by absorption. When degenerative processes take 
place the evidence of such is observed. 

Results. — If the circulation is completely stopped, necrosis of 
the part follows, and even gangrene when putrefactive organ- 
isms invade. 

Frequently, however, collateral circulation saves the part from 
injury in which event the thrombus may undergo resolution, or 
it may soften so rapidly that detached portions become emboli. 
Again thrombi may become fragmented, or whole thrombi de- 
tached, thus resulting in serious embolism. 

Hyaline degeneration with calcification may occur. Organiza- 
tion will often displace the thrombus, converting the vessel into 
a solid fibrous cord, or into an irregular channel with fibrous 
trabecular, the latter becoming covered with endothelium. 

Embolism 

Embolism is the transportation and lodgement of any substance 
within the circulation, capable of obstructing the flow of blood. 
Such substance (solid, liquid or gas) is called an embolus. 

Types of Emboli : 

I. According to location: 

1. Cardiac (rare) — a large venous thrombus, detached and 
doubling upon itself may occlude the pulmonary orifice in the 
heart, or a ball thrombus may plug the valves. 

2. Arterial — the most common emboli are found usually in 
small arteries or arterioles. The pulmonary branches are the 
most frequently affected, the embolus coming from a thrombus 
in the right side of heart, or venous system. Next to the pul- 
monary arteries, the following are affected in order of frequency: 
arteries of kidney, spleen, cerebrum (especially the middle cere- 
bral) and less often, or at least less often detected, in lower ex- 
tremities, upper extremities, liver, stomach, retina, and more 
rarely elsewhere. The emboli come from left cardiac and aortic 
thrombi or atheromatous ulcers, and rarely from the right side 
of the heart or venous circulation (paradoxical emboli). 

3'. Capillary — usually composed of tissue cells, bacterial cells, 
oil globules, gases, pigments (malarial) etc. Various metastases 
are thus explained. 



CIRCULATORY CHANGES 91 

4. Venous. — Since veins become larger in the direction of the 
blood current, embolism occurs in the systemic veins only when 
the venous blood current becomes slowed and momentarily and 
repeatedly reversed, or when a foreign body by its own weight 
gravitates against the blood stream. This is called retrogressive 
embolism. The portal vein narrows in the direction of the blood 
stream like an artery, hence emboli from the spleen, pancreas, 
gastrointestinal tract are frequently caught in the liver. They 
are often infective. 

5. Lymphatic — retrograde embolism occurs as in veins and ex- 
plains certain cases of metastasis to more distal points as can- 
cer of humerus from axillary glands. 

6. Paradoxical or crossed embolism occurs when emboli orig- 
inating in systemic veins or right auricle find their way to 
the arterial system. They pass through either a patulous fora- 
men ovale or when small through the pulmonary capillaries 
(which are larger and more dilatable than the systemic capil- 
laries). 

II. According to composition, emboli consist of: 

1. Fragments of thrombi — most frequent of emboli — and rarely 
whole thrombi; as from pelvic veins. 

2. Fragments of cardiac valves and vegetations. 

3. Calcareous and atheromatous matter from atheromatous ul- 
cers. 

4. Tumor cells and fragments (neoplasmic emboli) which have 
penetrated the vessel. 

5. Tissue cells, as from liver, placenta, chorion villi. Lym- 
phocytes and leucocytes infiltrate liver, etc.. in myeloid leucemia. 

6. Parasites. Animal (as filaria, echinoeoccus, etc.), and bac- 
terial emboli. By "septic emboli" is usually meant those in- 
fected with, or consisting chiefly of, pyogenic bacteria. Pyemia 
is thus caused. 

7. Extraneous matter, as oil globules from laceration of fatty 
tissue, including fractures or operations on long bones; pieces 
of bone in comminuted fractures ; bubbles of air, as may happen 
when veins are ruptured or cut as in operations, especially about 
the neck. All such emboli entering vessels through injuries are 
called traumatic. 



02 GENERAL PATHOLOGY 

Gaseous emboli may also occur from the activity of aerogenic 
bacteria, or in caisson disease, where from increased atmospheric 
pressure gases (chiefly N) may accumulate, and expand with the 
formation of bubbles on reduction of pressure. 

Results of Embolism. — Occlusion of valvular orifices, pulmo- 
nary artery or one of its main branches, one of the coronary ar- 
teries, or a large cerebral artery, usually causes sudden death. 

In smaller pulmonary branches, recovery may occur after a 
period of great dyspnea. When many small branches or capil- 
laries are plugged, death may ensue; fat or air embolism may thus 
be fatal. It is also thought that air in sufficient quantity can 
cause death by forming foam which interferes with the heart's 
action. 

In cases of small emboli, when single or few in number, col- 
lateral circulation usually relieves the part from degenerative 
change. If, however, the embolus lodges in a terminal vessel, 
an infarct results. 

Thrombi are apt to form upon emboli. If an embolus should 
not have completely occluded a vessel, the thrombus will stop 
the flow. 

Embolism often results in metastasis of malignant tumors, as 
sarcoma, and of infections, as "embolic abscesses" — pyemic, ame- 
bic, etc. 

Metastasis means the transportation of living material from a 
focus of disease, capable of reproducing the disease at the points 
of deposit. 

Infarcts 

Infarcts are more or less cone-shaped necrotic areas, caused by 
obstruction of the terminal or "end vessel" of a part (the latter 
being an artery having no collateral branches beyond the point 
where it breaks into capillaries). Occasionally the occlusion of a 
number of adjoining arterioles or capillaries causes infarcts of 
very irregular outline. 

The essential necrotic change in infarcts is coagulation nec- 
rosis, except in the brain where liquefaction necrosis develops 
from the start. 

Two forms of infarcts : (A) anemic or white, which are de- 
void of blood, and found most frequently in kidney, spleen, heart, 



CIRCULATORY CHANGES 93 

brain, stomach and intestine; and (B) hemorrhagic or red, which 
are infiltrated with blood, and found most frequently in lungs, 
less often in spleen, kidney, and other locations. 

Etiology. — Embolus or thrombus in a terminal artery. This, 
however, is not necessarily followed by infarction, as may be 
seen in lungs and liver, where there is free circulation. Nor need 
the occlusions always be in a terminal artery — infarcts may occur 
in intestines Avith free anastomosis. Again, hemorrhagic infarc- 
tion is said to occur by occlusion of a terminal vein. If the blood 
supply be too slowly occluded, collateral circulation will prevent 
infarction. 

The manner and sequence in which anemic and red infarcts 
develop have occasioned much discussion. Some claim that the 
anemic infarct is the first result of embolism, the red infarct, a 
secondary condition. Adami believes that the essential factor 
in formation of an anemic infarct is the rapid death and coagula- 
tion of the hemorrhage; should the death of part be slowly de- 
veloped, hemorrhage is permitted to occur (red infarct). Why 
anemic and red infarcts may be found at different times in the 
same organ depends chiefly on the condition of the cells at the 
time, for experimental ligation of the renal artery is followed by 
necrobiosis in one and one-half hours, but if some poison (diph- 
theritic toxin) be previously injected, it follows in three-quarters 
of an hour. 

Anemic infarcts develop usually in dense tissue, as kidney 
and hemorrhagic infarcts in loose tissue, as lung ; this has thus 
been explained : the capillaries around the necrotic area become 
congested (zone of hyperemia) and exude serum which infiltrates 
the cells in the immediate vicinity, causing compression of the 
capillaries and prevent the progression of blood into the necrotic 
area. In loose tissue the capillaries rupture, infiltrating the 
area with blood. The exceptional cases are explained by path- 
ologic variations in looseness or density of the tissues, as in fatty 
degeneration or in fibrosis respectively. 

An essential factor in infarct formation is smallness of 
the area involved; large areas suddenly deprived of blood be- 
come gangrenous. A possible explanation may lie in the fact, 
as Weigert claimed, that pervasion of an area with blood serum 



94 



GENERAL PATHOLOGY 



is necessary for coagulation necrosis — large areas can not thus 
be bathed before gangrene has set in. 

Gross Morbid Anatomy. — An anemic infarct is a cone-shaped 
or irregular whitish or yellowish area, softer than normal, with 
apex toward occluding vessel and base toward periphery, its 
outer surface depressed below the general surface of the organ. 
The red zone of hyperemia can usually be seen. 




Fig. 19. — Old anemic infarct of spleen. (Stengel and Fox.) 



The hemorrhagic infarct has the same shape and location as 
the anemic, but is red or dark in color, firmer than normal, and 
its surface elevated. Subsequent changes will alter the consist- 
ency in both forms. 

Microscopically.— Tn the anemic form, bloodless areas with co- 
agulation necrosis, fibrin or fibrinoid material, and necrotic cells 
are seen. Hemosiderin is sometimes seen and rarely hematoidin 
in the central parts. In the hemorrhagic form, blood cells with 
pigment and fibrin, also necrotic tissue cells are seen. 



CIRCULATORY CHANGES 95 

The occluding* embolus or thrombus may sometimes be seen 
grossly as well as microscopically in sections which pass through 
these occluding bodies. 

Results. — (1) The area may become encapsulated, and the con- 
tents undergo fatty change, calcification, caseation or liquefac- 
tion. 

It may be gradually absorbed and replaced by ingrowth of 
fibrous tissue, which subsequently contracts, forming a scar 
or cicatrix. 

Infection may take place when infarcts are so located as to 
be readily reached by microorganisms, as in lungs. Those 
caused by infective emboli are of course followed or associated 
with infectious processes. (Fig. 19.) 

Edema, Dropsy or Anasarca 

These terms signify an excess of fluid in the tissues or body 
cavities. The term edema properly applies to interstitial infil- 
tration of fluid in any pari: anasarca, to widespread subcuta- 
neous infiltrations; wheals, to small circumscribed cutaneous in- 
filtrations; dropsy, to fluids in cavities; transudation, to fluid 
poured out in noninflammatory conditions; and exudation, to 
fluid poured out in inflammatory processes. 

Etiology. — 1. Increased capillary blood pressure due to pas- 
sive congestion, pressure upon veins, etc. 

2. Increased permeability of capillaries, due to: 

(a) Alteration of blood, containing toxic substance as in in- 
fectious diseases. Bright 's disease, anemias, and cachexias. 

(b) Local disease of walls, as in inflammation. 

(c) Nervous influence, as in paralysis or disease of brain or 
cord, in neuralgia, and various nervous irritations. This may 
act by vasomotor depression, by trophic disturbance of intima, 
and in other ways not understood. 

3. Disturbed osmotic conditions. The tissue fluids may be 
hypertonic (contain more NaCl than the blood) causing tran- 
sudation in the effort to establish isotonicity. Increased NaCl 
content of the affected tissues has been demonstrated in cardiac 
and renal dropsies. 

4. Extensive obstruction of lymphatic vessels will prevent the 
normal removal of lymph, as in chylous ascites, in elephantiasis, 



96 GENERAL PATHOLOGY 

etc. In moderate obstruction, the venous capillaries can remove 
all the lymph. 

5. Decreased pressure in tissue, as when the space left by 
atrophy or destruction of tissue in brain or cord is filled with 
fluid (" edema ex vacuo"). 

In individual cases it is impossible to determine how many of 
these causal factors may be associated, or in some cases even to 
name the chief factors. 

We have the following types of edema : 

Cardiac — from weak heart action (passive congestion) seen 
in dependent parts, as ankles, wrists, hands, bases of lung, etc. 

Renal — from nephritis (seen in some forms, as acute nephri- 
tis), also in loose tissue (about eyelids). In other cases, it re- 
sembles cardiac edema. 

Cachectic — seen in loose tissue about eyelids, backs of hands, 
etc., may rarely be widespread. This is seen in malignant 
diseases. 

Mechanical — due to venous or rarely lymphatic obstruction. 

Toxic — often widespread and due to alterations of the blood 
as a result of toxins. 

Angioneurotic — as in some forms of urticaria, due to vaso- 
motor disturbances. 

Lymphatic — often widespread; the fluid sometimes is milky 
in appearance, due to presence of fat, mucoid substance, etc. 

Pulmonary edema — so called when the air cells are filled with 
fluid. 

Chemosis — subconjunctival edema. 

Dropsy in cavities is known as: 

Ilydrothorax, Hydropericardium, Hydro-peritoneum or Ascites, 
Hydrocele (in tunica vaginalis), External Hydrocephalus (in 
cerebral meningeal sac), Internal Hydrocephalus (in cerebral 
ventricles), External Hydrorrhachis (in spinal meningeal sac), 
Internal Hydrorrhachis or Syringomyelia (in central spinal ca- 
nal), Hydrops Articuli (dropsy of joints), etc. 

Gross Anatomy. — The part is swollen, tense and shiny on the 
surface, pale, pits on pressure, has a doughy consistence, and 
subnormal temperature (deficient circulation). On incision 
watery fluid escapes, which is usually clear, thin, pale or yel- 
lowish (sometimes red, greenish or milky) ; contains but little 



CIRCULATORY CHANGES 97 

fibrinogen and albuminous matter; specific gravity — 1.008 to 
1.014. Inflammatory fluid contains more albuminous matter and 
usually coagulates readily; specific gravity 1.018 to 1.020. The 
tissue infiltrated is firmer than normal. 

Microscopically. — Dropsical fluid may sometimes be seen in 
tissue, appearing homogeneous and electing the acid stain. In- 
flammatory edema is usually granular and contains a certain 
amount of cellular elements. The tissue cells are separated and 
may be hydropic or otherwise degenerated. 

Result. — Acute cases recover if the cause can be removed, 
though if very extensive (as in pulmonary edema) or in unfa- 
vorable location (as in edema of glottis), death may ensue. 

Where the condition is permanent or the cause can not be re- 
moved various forms of degenerations and fibrosis result. 



CHAPTER V 

INFLAMMATION 

Inflammation is a compound pathologic process represent- 
ing the reaction of tissues toward an irritant. 

Etiology. — Any mechanical, physical, chemical, infectious or 
nervous irritation, sufficient to cause local injury, but insuffi- 
cient to cause immediate extensive necrosis. 

Perhaps in all cases, the injured (degenerated or necrosed) 
tissue becomes the direct irritant, though some substances as 
toxins, etc., may also cause emigration of leucocytes by their 
chemotactic influence. 

Nervous irritation probably acts primarily through the vaso- 
motor nerves. 

The causes may be divided into external and internal — the 
latter being products of abnormal metabolism. Again we have 
simple, or noninfective, and septic, or infective, causes — the es- 
sential difference being that the simple are not reproductive, 
while the infective are constantly being reproduced and usually 
increased until the reparative processes overcome the destruc- 
tive, or death ensues. 

Inflammation is either (icntc — in which the vascular phenomena 
predominate; or chronic — in which the proliferative changes pre- 
dominate. 

Gross Pathology of Acute Inflammation. — Heat, redness, pain, 
and swelling (calor, rubor, dolor, tumor — of Celsus) are the 
chief general characteristics. (The distinctive features of the 
various types must be separately described.) 

Microscopically, the following histologic changes have been 
noted: The arteries and arterioles temporarily contract, but 
soon begin to dilate, and in "an hour or so" full dilatation of 
all the vessels is seen, with increased blood flow (hyperemia). 
Gradually the blood stream becomes slower, the corpuscles leave 
the central axial stream (in the larger vessels) and the leucocytes 
adhere to the vessel walls (marginatum). The endothelium be- 

98 



INFLAMMATION 99 

comes swollen and probably more adhesive, and the vessel more 
permeable. 

The first element which escapes from the vessels is the fluid 
of the blood (a transudation) ; later the fluid is found to be rich 
in albuminous substances which aid in proliferative processes, 
and this modified blood plasma with the blood cells which per- 
meate the area is called the inflammatory exudate. The leuco- 
cytes emigrate before the red blood cells pass through the vessel 
walls and in larger numbers, due to the positive chemotaxis which 
attracts them to the irritant. Ked blood cells always pass out of 
the vessels into the affected area (cliapedesis) but this is conspic- 
uous only in severe grades of inflammation. 

The leucocytes are chiefly of the polymorphonuclear (phago- 
cytic) variety, but in some cases especially in inflammation due 
to animal parasites, eosinophils are also found. In later stages 
lymphocytes abound, derived from Lymph channels and from 
proliferation of local lymphoid-tissue cells. Plasma cells, which 
are probably altered lymphocytes, with distinct and eccentrically 
placed nuclei, may be found in any type of inflammation. 

Proliferation of the fixed connective-tissue cells and the endo- 
thelium of lymph spaces and capillaries occurs sooner or later, 
thus forming "round cells" with large pale nuclei. At this 
stage many of the leucocytes have disappeared, but those that 
remain together with the lymphocytes and proliferated cells just 
mentioned constitute the so-called " round-cell infiltration." 
Some of the newly formed connective-tissue cells become "wan- 
dering cells" which are more or less phagocytic, while the re- 
mainder elongate and form fibrous tissue (fibroblasts). 

Degenerative changes are always present in varying degrees, con- 
sisting of cloudy swelling, mucoid or fatty degeneration, coagula 
tion necrosis, liquefaction or other necrosis. 

A typical, acute inflammation is therefore characterized by 

Hyperemia of the affected area, 

Exudation of serum from the vessels, 

Emigration of leucocytes, 

Diapedesis of red blood cells-, 

Proliferative changes in the fixed tissues, 

Degenerative changes. (Figs. 20, 21, and 22.) 

There are ten types of inflammation: 



100 



GENERAL PATHOLOGY 



I. Edematous or Serous. — In this type there is an excessive 
fluid exudation, with little tendency to fibrin formation, and 
relatively few cells, due to intense irritation, as of steam or cor- 
rosives; or to mild subacute or chronic irritation, as in serous 
effusions. 

II. Fibrinous. — The exudate is especially rich in fibrin factors, 
the fibrin appearing as fibrillar, granular or homogeneous de- 




Fig. 20. — Acute inflammation. (Mallory.) 




Fig. 21. — Inflammation of the mesentery, show- 
ing overfilling of the blood vessels, with emigra- 
tion of leucocytes and diapedesis of red corpuscles. 
(Ziegler.) 






mm 




^\ it «. r- 7>« # 










Fig. 22. — Acnte inflammatioi 
(Mallory.) 



posits. This type is seen most typically on serous surfaces, but 
it also occurs in tissues. 

III. Diphtheritic or Croupous. — This is essentially the same as 
the fibrinous, but with more pronounced coagulation necrosis 
of the cellular elements, thus forming a tough membranous pellicle 
— the false membrane. This type is met with most typically on 



INFLAMMATION 



101 



mucous surfaces, due to bacteria (as the diphtheritic bacilli, strep- 
tococci, etc.), steam, chemicals, etc. (Fig. 23.) 

IV. Suppurative. — Characterized by excess of leucocytes aud 
liquefaction of the exudate and fixed tissues. Clinically prob- 
ably always due to pyogenic organisms (usually pyococci, less 
often pneumococci, colon and typhoid bacilli, and other organ- 
isms) but injections of sterilized cultures, toxins, croton oil, tur- 
pentine, calomel, iodoform, etc., can also cause pus formation. 

The irritant being strongly chemotactic accounts for the ex- 
cessive local leucocvtosis. Enzymes liberated from the leuco- 




Fig. 23. — Pseudomembranous inflammation of the inula: a, a, masses of micrococci; b, b, 
necrotic cells; c, c, round-cell infiltration; d, d, fibrin network. (Ziegler.) 



cytes and probably other cells, and perhaps also in part by the 
bacteria, prevent fibrin formation, or liquefy what does form, 
together with the exudate and tissue, thus forming pus. 

Pus, is a yellowish, thick, usually alkaline (specific gravity 
1.020 to 1.040) fluid, containing pus cells in suspension. Pus 
cells consist chiefly of polymorphonuclear leucocytes, also a 
small number of proliferated connective-tissue and endothelial 
cells, all more or less degenerated (typically cloudy, swollen, 
clearing on adding acetic acid) or necrotic (shown by karyoly- 
sis, etc.) Pus may contain as many as 1,000,000 cells per c.mm.; 
1 oz. (30 c.c.) would thus contain nearly as many leucocytes as 
does the total amount of blood, illustrating the enormous cell 
reproductive power of the body tissues. 



102 GENERAL PATHOLOGY 

The fluid (liquor puris) contains proteins normal to blood, as 
well as derived proteins, albumoses, peptones, etc., also shreds 
of muscles, fibrous or elastic tissue variously degenerated, blood 
pigment, sometimes bacterial pigment, fatty acid crystals, cho- 
lesterin, etc. Bacteria may be present, free in the fluid or with- 
in the cells; frequently, however, the bacteria are destroyed by 
products of their own manufacture, or by action of the cells and 
exuded fluids. Such pus, as well as that caused to form by 
noninfective agents, is called " sterile pus." 

Suppuration may occur : 

Within tissues, as a circumscribed collection of pus (abscess) 
or as a diffuse infiltration (purulent infiltration or phlegmonous 
inflammation). 

On free surfaces, with considerable loss of tissue (ulcer). 

On serous surfaces or in serous cavities as an empyema. 

On mucous surfaces, as purulent catarrh, pyosalpinx, etc. 

Abscess Formation. — When a suppurative inflammatory area 
first liquefies in the center (which it does usually in forty-eight 
hours) an abscess is formed, i. e., a cavity filled with pus sur- 
rounded with a wall of inflammatory tissue, rich in leucocytes. 
The abscess grows by liquefaction progressing from within out- 
ward, the inflammatory Avail growing with equal pace. After 
sufficient time (four to ten days) granulation tissue (see Repair) 
forms. 

A fully developed abscess Avail therefore consists of an inner 
zone composed largely of leucocytes, exudate and intercellular 
matter about to liquefy; text a zone of inflammatory exudate 
with its granulations projecting into the preceding, and of con- 
gested capillaries (the source of leucocytes) hence called " pyo- 
genic zone," (formerly "pyogenic membrane"). The outer 
part of this zone, being the youngest part of the Avail, usually 
shows more fibroblasts and mitotic figures than the middle por- 
tion. 

Results. — The abscess travels in the direction of least resist- 
ance (called "pointing") which is usually toward the surface of 
an organ or part, because the pressure is less on that side and 
because there is greater vascularity on its inner side, hence 
more leucocytes and resistance. 



INFLAMMATION KM 

Rupture or incision of an abscess relieves tension and causes 
the fluid exudate in the abscess wall to flow toward and into the 
cavity, flushing out the tissue spaces of bacteria and toxic prod- 
ucts, and favoring protective (phagocytic, bacteriolytic and 
probably antitoxic) and reparative processes. 

In small abscesses or pustules, complete restitution may oc- 
cur; in larger ones, cicatrization follows healing (see Repair). 
Sometimes encapsulation, with inspissation or calcification, oc- 
curs. 

Death may ensue from intoxication when abscesses are very 
large or multiple, or when vital organs are involved, or when 
rupture occurs into large vessels, peritoneum, etc. 

In acute bacterial action, stasis is apt to occur in the vessels 
of affected areas (thrombosis and thrombophlebitis) thus prevent- 
ing hemorrhage even when eroded; but bacteria are also liable 
to grow into and through these plugged vessels and constitute 
one of the ways in which metastasis occurs. 

Special forms of abscesses: 

A Furuncle (boil) is a subcutaneous abscess, beginning in a 
sweat gland, sebaceous gland, or hair follicle. 

A Carbuncle is a similar but more extensive abscess, beginning 
in several glands or follicles simultaneously. Its favorite scat is 
in the back. 

A Pustule is a term properly applied to a suppurating vesicle, 
though often applied to any minute superficial abscess. 

Pyemia is a condition in which multiple abscesses exist through- 
out the body, due to emboli of pyogenic bacteria. 

An acute abscess is often called a "hot abscess," in contrast to 
the so-called "cold abscess," a term practically limited to lique- 
faction of tuberculous bone disease, as in lumbar vertebrae. 

Phlegmonous Inflammation. — This is a spreading inflamma- 
tion with a tendency to suppuration. In these cases "wall build- 
ing" characteristic of abscess is inadequate; the bacteria are not 
confined, the process spreads more or less rapidly, and metasta- 
sis is apt to occur through lymph and blood vessels. It is al- 
ways serious and sometimes attended with extensive loss of su- 
perficial tissue. 



104 



GENERAL PATHOLOGY 



An Ulcer is an area of superficial suppuration with erosion of 
the skin or mucous membrane. The floor of the ulcer is similar 
histologically to an abscess wall. Ulcers may be divided into: 

Phagedenic — rapidly spreading and destructive. 

Serpiginous — snake-like and irregular, healing on one side and 
progressing on another. 

Fungous — in which excessive granulation tissue forms. 

Indolent — in which granulation tissue is slow in forming. 

Gangrenous — in which putrefaction is an added feature. 

Follicular — small in extent as in crypts or follicles of glands. 




Fig. 24. — Tuberculous ulceration of the intestine. (Stengel and Fox.) 

Specific — due to tuberculous, syphilitic or other infection. 
(Fig. 24.) 

Peptic — due primarily to the digestive action of enzymes. 

V. Catarrhal Inflammation is inflammation of a mucous mem- 
brane, characterized by degeneration of epithelium (mucoid, 
fatty or necrotic) which is discharged with the abundant serous 
exudate upon the surface. The submucous tissue is infiltrated 
with a more or less serous exudate. (See Fig. 25.) 

When there are abundant leucocytes we have a purulent or 
mucopurulent catarrh. 

In chronic forms, productive processes lead to overgrowth of 
connective tissue, giving an appearance of hypertrophy of the 
mucosa. Later on, contraction of the fibrous tissue causes atro- 
phy. 



INFLAMMATION 



105 



Follicular Inflammation are terms applied to swollen lymph 
follicles, or to mucous glands (from obstructed ducts) the result 
of inflammation. 

VI. Parenchymatous Inflammation are terms used when the 
degenerative changes occurring in the parenchyma (or function- 




Fig. 25. — Acute bronchial catarrh, showing the escape of leucocytes from the submucous 
tissue between the epithelial lining cells. (Thoma.) 










:- 



4 *WJ&* 



r 



% 






Fig. 26. — Chronic interstitial nephritis: great increase of connective tissue around 
the glomeruli, renal tubules, and blood-vessels; from a case of arteriocapillary fibrosis. 
(Stengel and Fox.) 



106 GENERAL PATHOLOGY 

ating cells) of an organ are more conspicuous than the inflamma- 
tory changes in the interstitial tissues. 

VII. Interstitial Inflammation. — Strictly speaking, inflamma- 
tion proper occurs only in interstitial tissue, but the term is ap- 
plied to more or less chronic inflammation of an organ, attended 
by decided overgrowth of fibrous tissue. (Fig. 26.) 

VIII. Hemorrhagic Inflammation occurs when the diapedesis 
of red blood corpuscles is excessive, due to intense irritation. 

IX. Necrotic or Gangrenous Inflammation occurs when irrita- 
tion is intense or the body resistance is low, as cancrum oris. 

X. Productive Inflammation — when proliferative changes pre- 
dominate over the degenerative and other changes. Two types 
of productive inflammation may be considered: 

(1) When the framework of organs or tissues is especially 
proliferated, we have interstitial inflammation (see Type VII). 

(2) When loss of tissue is being replaced we have the phenom- 
ena occurring in repair of wounds, healing of abscess or ulcer, 
organization, etc. (A) Repair of Wounds. — (a) Healing by 
Immediate Union: When the margins of a very slight, clean 
wound are closely apposed, there is a minimum of capillary 
hemorrhage, the coagulation of which cements the margins of 
the wound together, holding them firmly so that repair work 
may proceed, which consists of a minimum of exudation, emigra- 
tion of leucocytes and cellular proliferation; the dead cells are 
removed by phagocytosis, liquefaction and absorption; the tissue 
cells and epithelial cells undergo division until the space is 
bridged over; the capillaries throw out bud-like processes from 
both sides which unite across the gap ; there are no new vessels 
formed, and no scar tissue produced. 

(b) Healing by First Intention: In larger aseptic wounds, 
the margins of which are more or less separated, and the gap 
filled with coagulated blood, the healing processes are the same 
as in (a), but there is greater inflammatory reaction and more 
cellular proliferation. New blood vessels are formed and fibrous 
tissue formation with cicatrization (scar formation) occurs. 

(c) Healing by Second Intention: This occurs when the gap 
between the margins is not filled with blood or exudate, and the 
margins are not approximated, or when the filled gap becomes 
infected and pus separates the margins, or when, as in an ulcer, 



INFLAMMATION 



107 



there is loss of surface tissue. Here new capillaries form to sup- 
ply nutriment for the extensively proliferating processes; then 
endothelial cells become swollen and send out solid protoplasmic 
processes, which unite with similar processes from the same or 
neighboring capillaries, thus forming loops which become cen- 
trally perforated to carry the blood; these loops as they project 
into the area of injury, covered with proliferated tissue cells, 
look like granules, hence the tissue is called "granulation tissue." 
This forms until all the lost tissue has been replaced. Contrac- 
tion of the fibrous tissue results in a scar of greater or lesser 
extent. (Figs. 27 and 28.) 

(d) When two granulating surfaces meet, as is well shown in 



- 





Fig. 27. — Loops of blood-vessels in granu- 
lation tissue. (Thiersch.) 



Fig. 28. — Formation of new blood-vessels as 
seen in the tail of a tadpole. (Arnold.) 



opposite walls of an abscess, or large gaping wound, the process 
is sometimes called "healing by third intention." 

(B) Adhesions between serous surfaces, organization of 
thrombi or other dead areas, healing through fragments of bone, 
ivory or sponge ("healing upon a scaffold") are all processes 
similar essentially to healing by first intention. The foreign 
body may be softened and absorbed, or encapsuled (surrounded 
by dense fibrous tissue). 

When repair processes are relatively extensive or prolonged, 
giant cells — "the giant cells of repair" are found. They origi- 



108 GENERAL PATHOLOGY 

nate either by division of nuclei without division of cytoplasm, 
or by confluence of cells. Many of them are phagocytic. 

Repair of a slight wound in avascular tissues, as the cornea, 
may occur directly by proliferation of the lost cells, without 
the essential phenomena of inflammation. 

Regeneration 

Regeneration is the formation of new tissue to replace that 
which has been lost. 

Physiologic regeneration occurs constantly either to counter- 
balance the loss from wear and tear, or to form new cells (in ex- 
cess of those destroyed) in the process of growth. 

Pathologic regeneration is often atypical and usually exces- 
sive. The etiology is not known. The cells have an inherent 




^k 



Fig. 29. — Fibroblasts forming fibrous tissue. (Ziegler.) 

tendency to multiply, with some restraining influence. In dis- 
ease there may be stimulation of reproduction by toxic products 
or other agencies, and a reduction of restraint by removal of pres- 
sure, etc. 

Pathologic Anatomy. — The cells swell, and multiply by mito- 
sis, or rarely by amitosis. The latter is supposed to be "a ret- 
rograde process in every instance." The cells subsequently 
form their characteristic intercellular substance. 

The less specialized a tissue may be and the younger the or- 
ganism, the more capable it is of regeneration, e.g., the connec- 
tive tissue of an organ will always outstrip the parenchyma, if 
the latter regenerates at all. 

Pathologic Regeneration. — In connective tissue, the cells swell 
and multiply by mitosis. The hcav cells are round or oval with 
paler nuclei than normal, and occur in great numbers; hence the 
tissue is said to have reverted to the embryonal type. The cells 



INFLAMMATION 109 

form intercellular substance or fibrils (i.e., they are "fibro- 
blasts") and later elongate and become relatively less numer- 
ous, as well as decreased in size. The polymorphonuclear leu- 
cocytes which infiltrate inflammatory areas, do not become con- 
verted into connective-tissue cells, and whether other types of leu- 
cocytes and endothelial cells do, is undetermined, though the 
budding processes of endothelial cells in the formation of new 
blood vessels seem to indicate the possibility of such conversion. 
(Fig. 29.) 
Epithelial cells are regenerated by mitosis, and usually in ex- 
















— " » — ' — — 

ion of epithelium. (Delafield and Prudden.) 



cess of those lost — the surplus being later degenerated and ab- 
sorbed. (Fig. 30.) 

Striated muscle cells regenerate to some extent, but rarely 
completely so. The destroyed area is first replaced by connec- 
tive tissue, into which the new muscle fibers grow. 

Smooth muscle fibers are probably never regenerated. 

Nerve fibers regenerate, but highly specialized cells as the 
multipolar cells of the cord do not, 

Fatty tissue begins with the formation of fat-free cellular tis- 
sue — later the cells become infiltrated with fat. 

Elastic tissue is capable of regeneration. 



110 GENERAL PATHOLOGY 

Cartilage may be regenerated, beginning from the perichon- 
drium, the proliferated cells of which (chondroblasts) are at first 
indistinguishable from fibroblasts. Fibrillar tissue first forms, 
which is later removed or becomes transparent and hyaline, thus 
forming cartilage. To a certain extent, the original cartilage 
cells near the line of injury also proliferate. "Very commonly, 
however, regeneration of fractures of cartilage is mainly fi- 
brous. ' ' 

Bone is also regenerated from the periosteum, the proliferated 
cells being indistinguishable from fibroblasts ; fibrous tissue 
forms, which later is infiltrated with lime salts (the cells now 
being called osteoblasts). Essentially the same process takes 
place from the marrow. The infiltrated tissue forms the callus 
or splint which holds the margins of fractured bones together, 
until the true osseous tissue is formed. 

Glandular tissue is but imperfectly regenerated, or not at all. 

Metaplasia is the direct conversion of one form of tissue into 
another, as when connective tissue becomes cartilage, bone or 
mucoid tissue ; or when epithelium changes from the columnar 
form to the squamous, as in covering of a healing ulcer in the 
trachea. Metaplasia is true only of tissues of the same type, 
e.g., epithelium can never become connective. 

Heteroplasia means production of a tissue within a part to 
which it is foreign, as when cartilage or bone forms in the pa- 
rotid gland, ovary or testicle. It is really metaplasia, since it is 
the connective tissue of the part which is converted into bone, 
etc. 



CHAPTER VI 

PROGRESSIVE TISSUE CHANGES 
Hypertrophy 

Hypertrophy is a simple progressive process, resulting in ab- 
normal increase of a part or organ. There are two types : 

(a) Simple hypertrophy is an increase in the size of the cells. 

(b) Numerical hypertrophy or hyperplasia is an increase in 
number of the cells. 

Both types are usually found associated (combined hyper- 
trophy). 

True hypertrophy is increase in size of all the tissues of which 
a part is composed, and the relationship of the parts is not ma- 
terially altered, as in hypertrophy of heart, uterus, etc. 

False hypertrophy or hyperplasia occurs, when one or other 
of the constituent tissues is alone increased, or in excess of the 
other parts. Examples are cirrhotic liver, fatty or amyloid in- 
filtration, the enlargement of muscles in pseudohypertrophic 
paralysis, etc. 

The term "hyperplasia" is loosely used as has been indicated, 
but is most commonly applied to increased production of con- 
nective tissue in a part or organ. 

Giant growth when general is not hypertrophy in a true sense, 
but rather an abnormality of development. Hypertrophy is a 
pathologic change occurring in a previously normal tissue. 

Etiology. — 

1. Repeated or intermittent pressure. 

2. Increased functional demand. It is called "work hyper- 
trophy" when due to increased exercise, and "compensatory 
hypertrophy" when an organ is called upon to do more work 
because of degeneration or destruction of a companion organ 
(as in kidney) or of other parts (as heart when vessels are dis- 
eased), etc. 

3. Nervous influence, as in hemihypertrophy (when one-half 
of face or body is hyper trophied). 

. Ill 



112 GENERAL PATHOLOGY 

4. Excessive eating and drinking. The heart is said to en- 
large from this cause. 

5. Obscure causes, as disturbance of certain internal secre- 
tions, e.g., acromegaly is associated with alteration in the pitui- 
tary body. 

In so-called physiologic hypertrophy, as of mammary glands in 
pregnancy, there is no existing increased work which causes the hy- 
pertrophy, but rather the anticipation of such work, and un- 
doubtedly depends upon nerve influence. 

Gross Pathology. — In true hypertrophy, the part is uniformly 
enlarged and consistence usually increased. In hyperplasia, 
the increase in size and consistence is apt to be irregular. 

Microscopically, the cells are increased in size or number or 
both. In hyperplasia, there is usually decrease of parenchyma, 
with increase of other tissue elements. 

Pathologic Physiology. — In true hypertrophy function is in- 
creased — as secretion, muscular power, etc. In hyperplasia, 
function is usually decreased. 

Results. — Hypertrophy always reaches a limit sooner or later, 
at which degeneration and atroplry usually set in. In some cases, 
as in enlarged thyroid, serious general disturbance results. 



CHAPTER VII 

TUMORS 

In the broad sense of the term, a tumor means any form of 
swelling of limited extent from a dislocated joint, pregnant uterus 
or hematoma to tumors proper and cysts. In the more restricted 
sense, however, as commonly used in pathology, a tumor may 
be thus denned: A tumor, or neoplasm, is an independent new 
growth, without known cause, true function, typical structure or 
definite limitation of growth. It is independent of external stimu- 
lation or functional demand in its development, and has an ade- 
quate vascular and nerve supply of its own. It does not increase 
function, as does hypertrophy, and the occasional secretions are 
apparently purposeless. It grows so long as the body can supply 
sufficient nourishment, and may grow rapidly even when the body 
is wasting. 

Tumors grow by numerical hypertrophy of cells normal to the 
body at some time or other in its development; no foreign ele- 
ments are introduced, i.e., tumors are not "heteroplasins." 

The structure of tumors is atypical, for while they retain 
certain characteristics of the parent tissues from which they 
spring, the arrangement and proportion of cells and stroma are 
atypical. 

Theories of Origin and Causation 

The Irritation Theory (Virchow). — This accounts for about 20 
per cent of tumors, as smokers' cancer of the lips, scrotal cancer 
of chimney-sweeps, sarcoma of injured bone, papillomata of anal 
and genital regions, etc. 

On the contrary, parts especially subject to repeated injuries, 
as the hands, feet, nipples, are rarely affected. 

The Inclusion or Embryoblastic Theory (Cohnheim). — During 
fetal development, embryonic cells are included in tissues where 
they remain quiescent as cell "rests" or "remnants," until some 
irritation starts proliferation. This theory explains dermoid 
cysts, certain carcinomata at points of epithelial transition, as of 

113 



114 GENERAL PATHOLOGY 

lips, cervix uteri, chondroid tumors in bone and sarcomata from 
pigmented moles, etc. 

However, many locations of complex developmental processes, 
as in the heart and nervous system, are seldom the seats of tumor 
growth. 

The Parasitic Theory (Paget). — This was suggested by the fact 
that many tumors give rise to metastasis, recur when removed 
or may be transplanted; also by reports that cancers have oc- 
curred in epidemics, or are contagious and hereditary, but chiefly 
by the fact that protozoon-like bodies resembling coccidia, par- 
ticularly in Paget 's disease of the nipple, have been found in 
certain tumor cells. Many of these bodies, however, are probably 
products of cell activity or cell degeneration, while transplanta- 
tion resembles skin grafting too closely to justify credence that 
parasites are a factor in tumor transplantation. 

The Habit of Growth Theory (Adami). — Cells have two func- 
tions — the performance of work and reproduction. During cell 
reproduction no work is performed, and vice versa. Irritation 
whether parasitic or otherwise may so modify the cell activities 
that reproduction becomes excessive and function diminishes or 
disappears. 

The Nervous Theory. — Thyroid tumors (goiters) seem to de- 
pend upon nervous excitement. Papillomata, as warts, are known 
to disappear by mental suggestion. "Omophobia" is a fear of 
tumors. 

The theories of Ribbert (disturbance of tissue tension), of 
Thiersch (of tissue equilibrium), of Billroth (diathetic — an ir- 
ritant in the circulation — which has never been demonstrated) 
and many others seem to be purely speculative. 

Predisposing Causes. — Age : Tumors occur more frequently 
after middle age. Of tumors occurring in early life the connec- 
tive tissue type is the most frequent; in early life the most fre- 
quent seats are the eye, kidney, bones and testicles. In adults 
and the aged, the stomach, uterus, liver and mammae are most 
frequently affected. 

Sex: Tumors in general occur twice as often in females as in 
males, although in regard to location, tumors of the stomach, 
tongue and lips are more frequent in males. 



TUMORS 115 

Heredity, occupation, race and climate are often said to be pre- 
disposing causes, but this has never been determined. 

The shape of tumors depends upon (a) the pressure of sur- 
rounding structures; (b) its consistence — the softer the tumor 
the more irregular; and (c) the part from which it grows; when 
growing upon a surface, it will form a tuberous growth (round 
top with broad base), polypoid (pendent with narrow pedicle), 
papillomatous (elongated with long narrow neck), (fungous) 
(large head and short thick neck), cauliflower (irregular projec- 
tions), dendritic (a highly branched cauliflower type), etc., and 
(d) the manner of growth — centrally or peripherally. When 
growing by proliferation at the center of the tumor, a uniform, 
round swelling or node forms, which often becomes encapsulated, 
the surrounding tissues being pressed aside. In peripheral 
growths, the surrounding tissues are infiltrated, the shape be- 
comes irregular, capsules are infrequent and metastasis frequent. 

Tumor growth is always accompanied by formation of new 
blood vessels which are usually thin and imperfectly formed. 

Metastasis takes place when tumors are highly vascular and 
cellular, and in those which are not encapsulated; it occurs via 
the blood vessels when these are in intimate contact with the 
tumor cells, as in sarcoma, or via lymphatic channels when these 
are in intimate contact with the cells as in carcinoma. Metastasis 
is also said to occur by direct extension over certain surfaces, as 
serous surfaces. Metastatic tumors are malignant, and malig- 
nancy means, in pathologic language, (a) invasion of tissues by 
infiltration, (b) ability to cause metastasis, (c) tendency to recur 
when removed, and (d) the injurious effects, other than mere pres- 
sure suffered by the patient, such as general anemia, or some 
form of intoxication. Such a condition is called cachexia. Sar- 
comata and carcinomata are the types of malignant tumors. 

Benign tumors are such as do not invade tissues, do not me- 
tastasize or recur when removed, but usually become encap- 
sulated and do harm only by their pressure upon other tissues 
or organs, or by gradually sapping the strength of the patient. 

A primary tumor is one originating at the site in which it is 
found. A secondary tumor is one originating by metastasis of 
cells (cell emboli) from a primary tumor. Primary tumors may 



116 GENERAL PATHOLOGY 

be multiple, but usually are single ; secondary tumors are almost 
invariably multiple. 

Degenerative changes occur in tumors as they do in the tis- 
sues from which they spring. 

Classification of Tumors. — Many different classifications have 
been suggested. In Virchow's Histogenetic classification, his 
law that " every tumor grows from previously existing cells of 
the same type" is made the basis of classification: (1) Histioid 
tumors — those growing from one kind of tissue only, as fibroma. 
(2) Organoid tumors — those growing from parenchymatous and 
connective tissues, as cancer. (3) Teratoid tumors (or syste- 
moid) — those made up of combinations simulating a system, as 
dermoid cysts. 

Cohnheim's embryoblastic classification divides tumors accord- 
ing to their epiblastic, hypoplastic or mesoblastic origin, but no 
note is here taken of the fact that many tumors similar in 
histology and function are derived from all the layers of the 
blastoderm, and vice versa. 

Adami's modification endeavors to remedy this defect, and is 
considered by Beattie and Dickson as the "most complete and 
scientific classification compatible with present knowledge." 
First the tissues, embryologically considered are divided into (a) 
lepidic ("rind") or lining membrane group, without lymph or 
blood vessels or stroma between the cells; and (b) hylic ("pulp") 
or body framework group. The tumors are divided in lepidomata, 
including the papillomata, adenomata, carcinomata and endothe- 
liomata, and hylomata, including neuromata, gliomata, sarcomata, 
myomata, fibromata and other connective-tissue tumors. 

The commonest and perhaps the most practical classification is 
that which is based upon the type of tissue involved : 

1. Connective tissue ; fibroma, myxoma, chondroma, osteoma, 
lipoma. Embryonic or malignant type — sarcoma. 

2. Muscle tissue; leiomyoma and rhabdomyoma. 

3. Nerve tissue; glioma and neuroma. 

4. Vascular tissue; angioma — hemangioma and lymphangioma. 

5. Epithelial tissue; papilloma and adenoma. Embryonic or 
malignant type — carcinoma. 

6. Teratomata or complex new growths. 



TUMORS 117 

Fibromata 

Fibromata are tumors composed of wavy bundles of connec- 
tive tissue. 

Etiology. — Some of these tumors result from injury or contin- 
ued irritation; the causation of others is obscure. 

The favorite seats are the subcutaneous and submucous tis- 
sues, periosteum, sheaths of tendons and nerves, uterus, ovaries, 
kidney, heart, dura mater, etc. 

There are two types of these tumors — the hard and the soft. 

Gross Pathology. — Hard fibromata vary in size from a minute 
point to a fist ; they are sometimes lobulated and frequently mul- 
tiple ; are pale, firm, cutting like leather. On section, surfaces 



-J N - 



Fig. 31. — Hard fibroma. (Warren.) 

show irregular bands or whorls of fibers, often resembling the 
grain in wood. They are usually encapsulated. 

A subvariety is the "painful subcutaneous tubercle," being 
about the size of a coffee bean, very firm and circumscribed. 

Fibromata of the uterus are a combination of fibroma and 
myoma, often called fibromyoma, or simply "fibroid." These 
may become very large, weighing fifty pounds or more ; are usu- 
ally multiple and very hard. 

Keloids are hard subcutaneous fibromata, of irregular star- 
like outline, not encapsulated, but tend to spread : they often look 
like the scars of burns, and usually arise from scars in those 
who manifest a congenital predisposition. Keloids occur oftenest 
in negroes. 



118 GENERAL PATHOLOGY 

Microscopically are seen dense, matted, fibrous bands with rel- 
atively few cells; blood vessels are few and have thick fibrous 
walls, but no muscular or elastic coat. When cut transversely 
the bundles have a granular appearance. (Fig. 31.) 

The soft fibromata are usually found in subcutaneous tissues 
and the submucous tissue of the pharynx and digestive 
tract. In gross appearance they are usually larger than hard 
fibromata, soft and pink on section. Frequently they are poly- 
poid in form. Microscopically a loose fibrillar network is seen, 
with stellate and spindle cells irregularly distributed and some- 
times in islands. The vessels have distinct walls. (Fig. 32.) 




Fig. 32. — Soft fibroma of the subcutaneous tissue. (Stengel and Fox.) 

Molluscum fibrosum (neurofibromatosis) is a soft fibromatoid 
growth occurring along the course of subcutaneous and submucous 
nerves. They range in size from a pinhead to an orange and 
are usually multiple. 

Degenerations. — These are the same as those which occur in 
normal fibrous tissues — hyaline, mucoid, fatty, calcareous and 
liquefaction. 

Results. — A fibroma is usually very slow in growth and benign. 
If very large it may cause pain or pressure symptoms, or even 
death from hemorrhage, exhaustion or absorption of degeneration 
products. Fibromata do not recur when removed, except keloids 
and certain polypoid new growths, though keloids may disappear 
spontaneously or upon continued pressure. 



TUMORS 



119 



Myxomata 

Myxomata are tumors composed of mucoid tissue. Mucoid tis- 
sue is the precursor of connective tissue in fetal life. 

Etiology. — Chronic irritation may cause some forms, but the 
etiology is obscure. Myxomata usually occur in adult life, but 
may be congenital. 

The favorite seats are the subcutaneous tissues, especially of 
the mammary gland; also submucous tissue, especially nasal; in- 
termuscular septa, nerve sheaths, brain and spinal cord. 

In gross appearance these tumors are pale gray or reddish 
white tuberous or polypoid growths, soft and gelatinous on 
section, exuding a mucous material on pressure. The groAvth 




Fig. 33. — Section of a myxosarcoma, a, myxomatous tissue; b, strands of cells; c, fibrous 

tissue. (Ziegler.) 

is usually well circumscribed and encapsulated, varying in size 
from a cherry to a walnut, though sometimes larger. Occasionally 
the growth is diffuse and noncapsulated. 

Microscopically, irregular stellate cells with long anastomosing 
processes are seen lying within a transparent or slightly granular 
material; the vascular supply is usually poor, though the vessels 
are large and thin walled. (Fig. 33.) 

Results. — The growth is slow and benign, but is often associated 
with sarcoma (myxosarcoma) or with cancer (carcinoma myxo- 



120 GENERAL PATHOLOGY 

mato'des) which is malignant. Hemorrhage may convert this 
form of tumor into a blood cyst. 

Chondromata 

Chondromata are tumors composed of cartilage. 

Etiology. — Irritation and tranma account for some cases. In 
others remnants of cartilaginous tissue deposited in abnormal 
places, as in the parotid gland, or left unconverted in the de- 
velopment of bone form the starting point for these tumors, while 
congenital predisposition and heredity also play a part. They are 
often associated with rickets, and are rare after puberty. 

Two chief types: (l)Ecchondromata (ecchondroses) are out- 




Fig. 34. — Chondroma of the thumb. (Warren.) 

growths from the perichondrium, occurring oftenest at the epi- 
physeal attachments of long bones, especially the phalanges of 
the hands, also at the interpubic and occipitosphenoidal junctions. 
They occur also as outgrowths from articular cartilages or syno- 
vial membranes in rheumatoid arthritis. (2) Chondromata, or 
enchondromata, originate in noncartilaginous tissues, usually 
bone, but also glandular organs as the parotid gland, testicle, 
ovary, and in muscles and tendons near their bony attachments. 
Gross Morbid Anatomy. — Chondromata are hard, resistant to 
the section knife, and vary in size from small nodes to large 
tumors. The ecchondromata are apt to be very irregular out- 
growths, often multiple, and firmly or loosely attached to the 
tissues from which they spring, and occasionally even detached. 



TUMORS 121 

The enchondromata are rounded growths, often lobulated when 
large, the lobules separated by connective tissue which carries the 
blood vessels. (Fig. 34.) 

Microscopically, the tissue resembles hyaline cartilage, less 
often white fibrous or elastic cartilage. The cells are less regu- 
larly arranged than in normal cartilage. Association with 
myxoma or sarcoma is frequent. Calcification or ossification also 
frequently occur. 

Results.- — These tumors are usually benign except when com- 
bined with sarcoma, but occasionally metastasis occurs even in 
pure chondromata, the secondary growths being found usually 
in the lungs. Degeneration with cyst formation is frequent. 

Chordomata 

Chordomata are tumors arising from the remains of the noto- 
chord or chorda dorsal is. They are found principally about the 
intervertebral disks and base of skull, and are seldom more than 
one-half inch in diameter. These tumors resemble cartilage gen- 
erally, but with "balloon-like" cells having small distinct nuclei, 
and apt to be vacuolated. 

Osteomata 

Osteomata are tumors composed of osseous tissue. 

Etiology. — Osteomata occur at any time of life; irritation and 
trauma account for some cases, and heredity seems to play a part, 
especially in the multiple osteomata of early life. 

There are two chief types: (1) Hyperostoses, which are in- 
flammatory outgrowths, including exostoses (wart-like out- 
growths) and osteophytes (flat, extensive and loosely attached 
outgrowths). These outgrowths spring from preexisting bone 
and are usually traumatic in origin. (2) Osteomata proper, which 
may spring from bone (homoplastic) or from nonosseous tissue 
(heteroplastic), such as the testicle, ovary, and meninges. 

Gross Pathology. — As in chondromata, a sharp distinction can 
not always be drawn between the inflammatory outgrowths and 
the true tumors, although the tumors are usually more rounded, 
more tumor-like in outline, and when large are apt to be lobu- 
lated. According to their density osteomata are (a) hard or 
compact, resembling the outer layer of long bones, and (b) soft, 



122 GENERAL PATHOLOGY 

cancellous or spongy, resembling the inner cancellous bony tis- 
sue with a shell of compact bone on the exterior. (Fig. 35.) 

A sub variety — eburnated (ivory-like) osteomata — consists of 
very hard and usually multiple growths, occurring on the inner 
table of the skull bones (here often syphilitic in origin), in the 
antrum of Highmore and elsewhere. 

Microscopically, these tumors resemble bony tissue, but the 
Haversian canals and blood vessels are usually quite irregular and 
smaller than in normal bone. 

Associations with chondromata, myxomata, fibromata, and sar- 
comata are frequent, and degenerative changes, as softening and 
necrosis, occur. 




Fig. 35. — Osteoma of the lower jaw. (Warren.) 

Odontomata 

Odontomata are tumors growing from the pulp of teeth, and 
are not strictly osteomata. 

Lipomata 

Lipomata are tumors composed of fatty tissue. 

Etiology — The etiology is not known. Usually they appear in 
adult or middle life, but sometimes in childhood and occasionally 
congenitally. 

Lipomatosis is a condition in which there is local diffuse fatty 
growth in certain parts. Obesity is the general increase of fatty 
deposits throughout the body. 



TUMORS 123 

The usual seats are the subcutaneous tissues of the back, shoul- 
ders, buttocks and limbs, also submucous and subserous tissues 
and the mammary glands. 

Gross Pathology. — A lipoma is a circumscribed, encapsulated 
tumor, usually lobulated with connective-tissue septa. On the 
exterior, the new growths are somewhat hemispherical, rarely 
polypoid, and movable. They vary in size, and may become 
enormous. In the interior of the body they are usually polypoid, 
and occasionally found detached. 

Microscopically, lipomata resemble fatty tissues in general, al- 
though the cells are larger, and large thin-walled vessels are 
seen. 

Results. — These tumors are benign, although recurrence may 
take place after removal. Calcification and less often softening 
occur. The fat of lipomata is not used by the system in starva- 
tion. 

Sarcomata 

Sarcomata are tumors composed of connective tissue of the em- 
bryonic type, having very little intercellular substance and a 
large number of cells. 

Etiology. — These tumors occur in youth and early adult life, 
and are sometimes congenital. Some cases follow traumatism. 
They are more frequent in males. 

Locations. — Sarcomata are found in the subcutaneous, perios- 
teal, tendinous, and muscular tissues; in bone, cartilage, lymph 
glands, submucous and subserous tissue ; in the kidneys, liver, 
spleen, thyroid, testes, etc. 

Gross Pathology. — Sarcomata are more or less rounded, usually 
without demarcation between them and the surrounding tissues, 
although when fully developed, or when growth is slow, a cap- 
sule or apparent capsule may form. Superficial tumors are apt 
to be flat or irregular elevations; typically a sarcoma is flesh- 
like in appearance when sectioned, pink in color, though many 
are pale or gray. Dilatation of blood vessels may cause a hemor- 
rhagic appearance, and actual hemorrhages into the tumor are 
frequent. Sarcomata infiltrate adjacent tissue and are not readily 
movable. They may be hard or soft according to the relative 
amounts of cells and intercellular substance. A whitish liquid 
exudes on section. 



124 GENERAL PATHOLOGY 

Pathologic Histology.— The cells are round, cylindrical, spin- 
dle-shaped, or polymorphous, and contain large vesicular or gran- 
ular nuclei. Mitotic figures may be seen in rapidly growing 
tumors — less commonly amitotic division occurs. Nuclear de- 
generation is frequent. The cells are irregularly arranged, though 
occasionally in more or less parallel columns. The intercellular 
substance is scant, homogeneous with few or no distinct fibers, 
and found in immediate relation with the cells, thus differing 
from carcinoma. 

The blood vessels usually consist of a single endothelial coat, 
though in some cases they are more fully developed and form 
the skeleton of the tumor; they penetrate the tumor tissue and 
come in direct contact with the cells (again differing from car- 
cinoma) — in fact, parts of the tumor may grow into the vessels 
permitting the blood to circulate in clefts among the tumor cells ; 
hence sarcomata metastasize through the blood vessels as a rule, 
while carcinomata which have more distinctly formed blood ves- 
sels metastasize through the lymphatics. 

Association with other tumors, especially of the connective 
type is frequent. 

Results. — Sarcomata are malignant as a rule. The round-celled 
and melanotic are the most malignant — the giant-cell and fibro- 
sarcomata are the least malignant, In general the smaller the 
tumor cells, the more malignant the tumor. Degenerations, as 
myxomatous, liquefaction, blood cysts, etc., occur frequently. 
Anemia, leucocytosis and fever often attend the disease. 

Sarcomata are classified as follows : 

1. Round-celled sarcomata — both large-celled and small-celled, 
including lymphosarcomata, most of the alveolar sarcomata, an- 
giosarcomata and sarcomatous cylindromata. 

2. Spindle-celled sarcomata — large-celled and small-celled, in- 
cluding a few alveolar sarcomata. 

3. Melanotic sarcomata. 

4. Giant-celled sarcomata. 

Round-celled Sarcomata 

Round-celled sarcomata are usually found in loose connective 
tissues in viscera, as kidney, ovary, brain, lymphatic nodes, etc. 



TUMORS 125 

Grossly tliey are white, gray or pink, soft, usually rounded 
and well-defined but not encapsulated; they bleed easily, are 
often quite soft and cheesy in the center, the small-celled being- 
softer than the large-celled tumors. 

Histologically, the cells when small resemble lymphoid cells. 
There is no fundamental difference between the small-celled and 
large-celled varieties; in the latter the cells are larger with rel- 
atively more cytoplasm, the nuclei stain less deeply, the inter- 
cellular substance is more fibrillar, and the blood vessels are fewer 
but better supported than in the small-celled variety. 

The lymphosarcoma is a small round-celled sarcoma occurring 
in lymph nodes, lymph adenoid tissue, and sometimes in other 
organs, as the thyroid, thymus and salivary glands. It resembles 
a lymph node in appearance and structure, the chief distinguish- 




Fig. 36. — Small round-celled sarcoma: in the center is seen a blood vessel with its wall 
of endothelium. (Stengel and Fox.) 

ing feature being its tendency to spread beyond the capsule or 
normal limitations of the nodes or organs, and in case of the 
lymph nodes, causing the separate nodes to fuse together, ob- 
literating the normal appearances, as germ centers, cortex, and 
medulla. 

The alveolar sarcoma is grossly similar to other forms of sar- 
coma and occurs mainly in lymph nodes and serous membranes, 
moles of the skin, warts, etc. Histologically there are trabecu- 
lar of spindle-shaped cells and intercellular substance, dividing 
the tumor into alveoli containing round sarcoma cells. Blood 
vessels traverse the trabecular and rarely if ever enter the cell 
groups. These tumors are difficult to differentiate from car- 
cinomata, though in the latter the blood vessels are said to be 
usually better developed. 



126 



GENERAL PATHOLOGY 



Angiosarcomata spring from the adventitia of blood vessels. 
They occur in the salivary glands, serous membranes, and in the 
skin, and consist of round-celled masses surrounding the blood 
vessels. These tumors are more or less benign, but often become 
melanotic and malignant. 

"Cylindroma" originally meant any tumor "showing gelat- 
inous masses or trabecular traversing its substance," but dif- 










Fig. 37. — Large round-celled sarcoma. (Delafield and Prudden.) 




Fig. 38. — Alveolar sarcoma. (Warren.) 



ferent histologic structures are described under this name. Sar- 
comatous cylindromata may be denned as sarcomata in which 
hyaline and myxomatous degeneration have occurred in more or 
less insular collections; also as angiosarcomata with similar de- 
generation of the sarcomatous cells surrounding the vessels, re- 
sulting in either case, in branching cylinders of gelatinous ma- 
terial throughout the tumor. (Figs. 36, 37, and 38.) 



TUMORS 



127 



Spindle-celled Sarcomata 

Spindle-celled sarcomata occur in dense tissues, as periosteum, 
tendons, fasciae, less often in loose tissues. Grossly, they are 
harder than the round-celled tumors, and more grayish and flesh- 
tinted. The cells are spindle-shaped with tapering ends and 
sometimes branching extremities, and apt to be arranged in par- 
allel rows. In the small-celled variety, the intercellular sub- 
stance is less fibrillar and the blood vessels more imperfect than 
in the large-celled form. (Fig. 39.) 

When the intercellular fibrils become very evident, it is called 




Fig. 39. — Spindle-cell sarcoma of the mammary gland. Oc. 3; ob. 9. (McFarland). 



fibrosarcoma, 
comata. 



The so-called "recurring fibroids " are fibrosar- 



Melanotic Sarcoma, or Melanomata 

Melanotic sarcomata, or melanomata, spring from some pig- 
mented tract, as the uveal tract of the eye, pigmented mole, etc. 
The cells contain metabolic pigment (melanin) varying greatly 
in amount, and distributed uniformly or in patches. The nuclei 
are poor in chromatin and show a distinct network. These tu- 
mors are very malignant, metastasize to any tissue, but chiefly 



128 GENERAL PATHOLOGY 

through the lymphatics to the lymph nodes. Sometimes the cells 
are epithelioid and arranged in alveoli. 

Giant-celled Sarcomata 

Giant-celled sarcomata are composed of spindle or round cells 
with a variable number of giant cells. The}- spring from the 
medulla of long bones, are circumscribed, and usually encap- 
sulated; may be firm or soft, reddish-brown on section and some- 
what fibrous. They occur oftenest in the young, at the lower 
end of the femur, upper tibia, lower radius and lower jaw (one 
form of epulis). (Figs. 40, 41, 42 and 43.) 

Two rare forms of connective tissue tumors are: 



® |>1 # ^ # f) ^ -/ " M^ > 







Fig. 40. — Large spindle-celled sarcoma. (Delafield and Prudden.) 

1. Xanthoma, which is a lipoma with large fat cells and a 
certain amount of round-celled infiltration, and of a peculiar 
yellowish color ; is found usually about the eyelids, and occa- 
sionally in diabetes, more generally distributed. 

2. Chloroma, which is a variety of lymphosarcoma or round- 
celled sarcoma, occurring in the periosteum of the bones of the 
head, especially the orbit, and having a peculiar greenish color; 
it is malignant, giving rise to secondary tumors in lymphadenoid 
tissue and especially the bone marrow. 



TUMORS 



I2y 




Fig. 41. — Melanosai 



itengel and Fox.) 







Fig. 42. — Giant cell sarcoma of the thigh, a, giant cells; &, spindle cells. (McFarland.) 



130 GENERAL PATHOLOGY 

Rhabdomyomata 

Bhabdonryomata are tumors containing striped muscle tissue. 
They are rare and usually congenital. In the genitourinary sys- 
tem, they are probably due to the inclusion of lumbar muscle 
fibers. Their favorite seats are the kidneys, testicle and other 
parts of the genitourinary tract, also heart muscle, lumbar and 
gluteal muscles. The tumors are round or irregular in shape 
and more or less encapsulated, and if superficial, pedunculated. 
Microscopically the muscle fibers are imperfectly developed and 




Fig. 43. — Metastatic melanosarcoma of lung, showing pigmented and nonpigmented nod- 
ules (from a specimen in the possession of Dr. Allen J, Smith.) 

associated with a varying amount of connective tissue. When 
the latter becomes embryonal in type, a rhabdosarcoma develops, 
which is much more frequent than the pure rhabdomyoma. 

Leiomyomata 

Leiomyoma! a are tumors containing smooth muscle fibers. 
They spring from preexisting smooth muscle, usually of an organ 
or the media of blood vessels. In the uterus it may arise from 
congenitally misplaced portions of the Wolffian body or ducts of 
Mueller. 



TUMORS 



131 



The favorite locations are the uterus, gastrointestinal tract, 
ovaries, less often blood vessels, skin, nipples, etc. 

Gross Pathology. — The tumors are firm, rounded, nodular masses, 
closely resembling fibromata, but usually darker in color, 
and varying in size up to many pounds. The large tumors are 
usually a combination of myoma and fibroma — a fibromyoma, 
such as the uterine "fibroid" which may grow to an enormous 
size. Leiomyomata are encapsulated, and on section have a 



£ 




} 1 




V 



Fig. 44. — Submucous fibroid in the uterus. The tumor forms a large mass in the in- 
terior of the organ whose wall is much attenuated at the fundus. The cervix is nearly- 
normal in size, though somewhat altered in shape. The ovaries and tubes which are still 
attached are normal. (McFarland.) 



striated appearance, the striae being concentrically arranged or 
in a wave-like manner. They are usually grayish or flesh-colored, 
but may be red, due to dilated blood vessels. 

Uterine fibromata are usually multiple, and either submucous, 
interstitial (intramural), or subserous in origin. The intramural 
tumors do not, as a rule, project from either surface of the uterus. 
Uterine fibromata occur oftenest during the third or fourth dec- 



132 



GENERAL PATHOLOGY 



ades of life, and continue to increase in size up to the time of 
the menopause, thereafter usually decreasing. (Fig. 44.) 

Leiomyomata of the skin occur in young adults, or even in 
children. They are multiple and often painful. 

Histologically, bundles of muscle cells are seen, running in dif- 
ferent directions and having cylindrical nuclei. Sometimes elas- 
tic tissue elements are present, and nearly always connective 
tissue cells. Blood vessels are scant, though often with well de- 
veloped middle coats. Calcification is common, especially in 
uterine fibromata ("womb stones") preceded by hyaline or fatty 
change. 

Results. — Growth is slow and the tumors are benign, although 
sarcomatous change may add a malignant character. 




Fig. 45. — Glioma of the brain. (Dclaficld and Prudden.) 

Glioma 

Glioma is a tumor composed of neuroglia. 

The favorite seats are the brain and cord, optic tract, nerve 
and retina, and parts of the olfactory tract. Glioma of the retina 
occurs usually between the second and fourth year of life. (Fig. 
45.) 

Gross Pathology. — Gliomata are usually single, rounded masses, 
gradually merging into surrounding tissue. Somewhat harder 
than brain, their color is but slightly changed, though some- 
times dark red. They vary in size from a pea to a lemon. Glioma 
of retina may extend to eyeball or along optic nerve. 

Pathologic Histology. — Great numbers of cells are seen with 
round or oval nuclei and with scant cytoplasm (glia cells). They 
are usually larger than the normal neuroglia cells. Fine wavy 
fibrils (neuroglia) lie parallel to the axes of the cells to which 



TUMORS 133 

they are attached at the sides, the ends of the fibrils being free. 
In the retina, the cells are similar to its granular layer. 

Results. — Benign, but may be dangerous from pressure or loca- 
tion. Glioma of eye may recur after removal. 

Glioma Ganglionare, or Ganglionic Glioma, or Neuroma 

This is a mixed tumor composed of neuroglia, nerve fibers, and 
ganglionic cells. It usually occurs in multiple nodular growths 
throughout the brain and cord, or in the sympathetic ganglia, 
varying in size from that of a millet seed to that of an apple. 

Gliomatosis is a diffuse proliferation of glia throughout the 
central nervous system. 

Neuroma occurs in two forms — true and false. 

True neuroma is a very rare tumor composed of nerve fibers. 

False neuroma (the common form) is a fibrous tumor spring- 
ing from the perineurium and endoneurium of nerves. 

The etiology is not known, though traumatism accounts for 
amputation neuromata. They are usually found upon the periph- 
eral nerves, but may occur in any part. Sometimes the nerves 
are involved near their roots, or at their endings within organs. 

Gross Pathology. — False neuromata are usually found as mul- 
tiple thickenings along the course of nerves. They may occu 
in the form of a network (plexiform neuromata). After ampu- 
tation small, rounded growths occur at the ends of some of the 
nerves, are firm and not sharply circumscribed. 

Pathologic Histology. — False neuromata are composed of re- 
ticulated connective tissue, pushing aside or surrounding the 
true nerve fibers — the latter being often degenerated from pres- 
sure. True neuromata are composed of medullated fibers (myelinic 
neuromata) or of nonmedullated (amyelinic neuromata). Ampu- 
tation neuromata are usually a mixture of myelinic and false 
neuromata. 

Results. — These tumors usually cause pain. They are benign, 
though often rapid in growth. 

Angiomata 

Angiomata are tumors composed of, or following the type of, 
blood or lymph vessels. Used alone, "angioma" refers to the 
hemangioma. 



134 



GENERAL PATHOLOGY 



Hemangiomata, or angiomata, are tumor-like formations con- 
sisting principally of dilated and elongated blood vessels, some 
of which may be independent new growths. A certain amount 
of connective tissue is always formed which holds the vessels to- 
gether. Usually the angioma is connected with the general circu- 
lation through a few, sometimes but one, arterioles or veins. 
Three forms are described: 

(a) Angioma simplex, or Nevus, which consists of dilated capil- 




K&. 






2&3w . 










• 






Fig. 46. — Cavernous angioma of liver. The illustration shows tumor tissue only: a, 
blood channels filled with corpuscles; b, fibrous framework supporting delicate walls of 
blood sinuses. (McFarland.) 

laries, arterioles and venules woven into a plexus. It is usually 
congenital (birthmarks). It may be red in color (arterial) or dark 
(venous) ; pigmented (pigmented mole) or covered with fine hairs. 
It may be found on the skin, lips, tongue, conjunctivae and rarely 
the meninges. 

(b) Cavernous angioma, or cavernoma, which consists of widely 
dilated blood cavities separated by connective tissue partitions and 
lined by epithelium. It is dark in color, larger than the simple 



TUMORS 135 

form, and may pulsate. It is found most frequently in the liver, 
where it may be multiple, skin, breast, bones and internal organs. 
(Fig. 46.) 

(c) Plexiform angioma, which consists of a dilatation and elon- 
gation of a group of arteries of moderate size, and found upon the 
head, face, perineum, legs, forearm and elsewhere. It is in reality 
a "congeries of cirsoid aneurysms" forming a tumor-like enlarge- 
ment. 

Lymphangioma is a tumor-like formation, consisting of dilated 
lymph vessels, rarely of newly formed lymph channels. Three 
forms are described: 

(a) Lymphangioma simplex, or lymphangiectasis, is a simple dila- 
tation of a group of lymph vessels forming tumor-like masses. A 
congenital forms occurs usually upon the face and neck, and often 
confined to the papillary layer of the skin. The acquired form is 
due to lymphatic obstruction (as elephantiasis, due to filarial) 
tending to dilatation of the lymph vessels and overgrowth of con- 
nective tissue. 

(b) Cavernous lymphangioma, which corresponds to the caver - 
noma of the blood vessels. It may affect the tongue (macroglos- 
sia) or lip (macrocheilia) or the mesentery. These conditions are 
congenital. 

(c) Cystic lymphangiectasis } which occurs commonly about the 
neck, as cystic hygroma, consisting of multiple clear cysts lined 
with endothelium and having fibrous walls. 

Among special forms of lymphangiomata may be mentioned 
the common pigmented mole, which is a slightly elevated growth, 
soft and flabby, occurring on the skin in early youth. It is a 
cutaneous outgrowth consisting of a stroma of fibrous tissue and 
containing pigmented cells. When consisting of telangiectatic 
vessels, it is called a pigmented nevus. 

Papillomata 

Papillomata are tumors growing from the papillary processes, 
which they resemble in structure. 

Etiology. — Irritation is the cause of many, if not all, of these 
tumors. They are found in the skin of the back, neck, and 
hands, the mucous membranes, particularly of the bladder, nose, 
larynx and gastrointestinal tract, and glandular ducts, as the 



136 GENERAL PATHOLOGY 

female breasts. They also occur within cavities of cystic adeno- 
mata (papuliferous cysts). 

Gross Pathology. — Various forms are described: (1) Hard 
fibromata, verrucce or warts, occur singly or in groups upon the 
skin. They may be smooth or cauliflower-like in outline, varying 
in size from a pinhead to a walnut. (2) Venereal warts or con- 
dylomata acuminata. These occur about the genitals and anus, 
rarely elsewhere, are softer, more vascular, and more polypoid 
than the ordinary warts, and caused by gonorrheal discharges. 
The condyloma latum, or mucous patch, is also a warty outgrowth 
upon mucous membranes and moist dermal surfaces, occurring 
during secondary syphilis. (3) Soft papillomata are usually seen 
on mucous surfaces as soft cauliflower-like growths, red, or gray 
in color, or sometimes as villous outgrowths. (4) Intracystic papil- 
lomata are villous outgrowths springing from the walls of cysts, 
especially mammary, thyroid and ovarian cysts. The growths 
may fill and greatly distend the cysts and occasionally rupture 
them. 

Pathologic Histology. — The normal relation of cells to the 
membrana propria persists in all papillomata. There is a cen- 
tral stroma which contains the vessels and is covered with 
epithelium — stratified squamous in case of skin growths, tend- 
ing to horny change and sometimes horny concentric whorls or 
pearls. The structure in the mucous membrane is the same 
where the epithelium is of the squamous type, as in parts of the 
larynx, but there is little tendency to horny change. In the 
gastrointestinal tract and bladder, the growths are soft and vil- 
lous or dendritic, and the epithelium is scant and of the type 
peculiar to the location. The relative amounts of connective tis- 
sue stroma and covering epithelium vary; when the latter pre- 
dominates, it may suggest an epithelioma, though papillomata 
always tend to grow outward rather than into deeper structures. 
Many of the soft papillomata are quite vascular and bleed easily. 
(Figs. 47 and 48.) 

Results. — Papillomata are benign, but large tumors may im- 
pair health by repeated hemorrhages, as in the gastrointestinal 
tract, or by interfering with function, as in bladder or larynx. 



TUMORS 



137 




Fig. 47. — Papillomata of the vocal cords (from a specimen in the Museum of the Phila- 
delphia Hospital). 




Fig. 48. — Papilloma of the scalp. The branching fibrous stroma is covered by an abnor- 
mally thickened, irregular epithelium. (Boyce.) 



138 



GENERAL PATHOLOGY 



Adenomata 

Adenomata are tumors resembling in structure an epithelial 
gland and developing from glandular epithelium. 

Etiology. — They are caused by irritation, as in gastrointestinal 
adenomata, by tissue inclusions, as in renal adenomata. In 
other cases the causes are obscure. 

Their favorite seats are the mucous membrane, especially of 
the pylorus, duodenum and rectum; the skin — sebaceous and 




Fig. 49. — Adenoma of the mammary gland, with cystic enlargement of acini and abundant 
interglandular hyperplasia of connective tissue. (Stengel and Fox.) 

sweat glands; certain organs, as the mammary glands (the most 
frequent seat), liver, kidney, adrenals, thyroid, ovary and uterus. 
Gross Pathology. — Adenomata occur as more or less diffuse, 
sessile growths, sometimes pedunculated or papillomatous in 
form; or within organs as nodular tumors, firm, usually single 
and encapsulated, capable of being shelled out, though at times 
adherent. On section the cut surfaces usually bulge and 
resemble, more or less, the parent gland, being grayish pink 
in the mammae, and red in the thyroid gland. 



TUMORS 139 

Pathologic Histology. — Acini with single layers of columnar 
epithelium (sometimes several layers) are seen enclosed by con- 
nective-tissue reticula, which contain the blood vessels. The ex- 
cretory ducts are absent or poorly developed. 

When the tissue corresponds closely to the normal arrange- 
ment, the tumor is a simple adenoma; when the stroma pre- 
dominates, fibroadenoma ; when acini greatly predominate, acinose, 
racemose or alveolar adenoma; when ducts are conspicuous, tubu- 
lar, or canalicular adenoma. 

Results. — Pure adenomata are benign, but may sometimes cause 
metastasis, especially the hepatic and thyroid tumors. General 
health may suffer from hemorrhages, interference with vital func- 
tions, or from ulcerations. Gastric and uterine adenomata are 
apt to become carcinomatous. (Fig. 49.) 

Carcinomata 

Carcinomata are tumors embryonal or atypical in character, 
which always arise from epithelial cells. 

Etiology. — Irritation accounts for some cases. They occur usu- 
ally after middle life, being rarely found in early life or child- 
hood. They are more frequent in women, and in the Caucasian 
race. Tumors springing out of connective tissues, as bone, can 
only be explained by the inclusion theory. 

The favorite seats are the uterus, skin, esophagus, pylorus, rec- 
tum, mammae, ovaries, less often the liver, kidney, thyroid gland, 
prostate and testicle. Carcinomata, however, may spring from 
any epithelial tissue. 

Secondary tumors usually do not affect the parts in which 
the primary growths are frequent, and occur usually in the lymph 
glands, liver, spleen, lungs, serous membranes, and bones. 

General Structure. — The cells are very diverse in outline — 
round, oval, squamous, fusiform, cylindrical, cuboidal or cau- 
date, and have large, clear nuclei. Compression develops poly- 
hedral forms. 

The stroma consists of fibrous tissue, which forms irregular 
spaces, or alveoli, which communicate with one another, within 
which lie the cancer cells in branching or anastomosing columns, 
due probably to the fact that cancer cells proliferate along the 
lymph channels. The stroma may be infiltrated with leucocytes 



140 GENERAL PATHOLOGY 

and plasma cells and even mast cells. In slowly growing tumors the 
stroma is fibrous; in rapidly growing tumors it approaches the 
embryonal or mucoid type. The stroma contains the blood ves- 
sels, which have distinct walls and do not penetrate the alveoli. 
The lymphatics are continuous with the alveoli, thus affording a 
ready means of metastasis. 

In general, skin cancers resemble enlarged papillae penetrat- 
ing into the tissues, and gland-celled cancers resemble acini of 
glands, filled with many layers of cells, but in all cases, there is 
noted the tendency of the cells to penetrate the basement or 
limiting membrane and infiltrate the tissues. 

Secondary carcinomata are usually multiple, more circum- 
scribed and less infiltrating, and as a rule softer than the primary 
tumors. 

The histologic differentiation between carcinoma and sarcoma 
can not always be made from the morphology of the cells, for 
they are polymorphic in both forms of tumor, and it finally rests 
upon : 

(a) Grouping of the cells — in alveoli in cancer; irregularly in 
sarcoma. 

(b) Intercellular fibers — none in cancer; always a few in sar- 
coma. 

(c) Position of blood vessels — in trabecula3 in cancer; among 
the individual cells in sarcoma. 

In alveolar sarcoma, however, these distinctions are not so 
evident, but here the intercellular fibrillar may be seen to be con- 
tinuous with the perialveolar fibrous tissue, and the blood ves- 
sels are thin-walled and not so well supported as in cancer. 

Degenerative Changes. — These are frequent, especially fatty de- 
generation. The cells may be cloudy, swollen, dropsical or vacuo- 
lated. Nuclear degeneration may occur, giving the appearance 
of parasites. True colloid degeneration may occur but is very 
rare, the term "colloid cancer" usually refers to myxomatous 
change of the stroma. Liquefaction may form cysts. Calcifica- 
tion occurs, especially in ovarian cancers. 

Inflammatory changes are common. On free surfaces, ulcera- 
tion results from traumatism, irritation or infection. Erysipelas, 
tuberculosis and syphilis may be associated. Hemorrhages are 
frequent both into the stroma and from the ulcerating surfaces — 



TUMORS 141 

the latter are apt to be extensive in cancer of the stomach and 
uterus. 

Malignancy. — Cancers are malignant ; the medullary giand- 
celled being most, the squamous-celled the least malignant. Me- 
tastasis occurs through the lymphatics, but occasionally through 
the blood vessels (veins) especially through the portal vein to 
the liver in cases of intestinal carcinomata. Hemorrhages, hem- 
olysis, and probably some form of toxemia cause the anemia and 
cachexia so characteristic of these tumors. 

Carcinomata are divided into: 

1. Epitheliomata, or squamous-celled carcinomata. 

2. Gland-celled carcinomata: 

(a) Adenocarcinomata. or cylindric-celled carcinomata. 

(b) Hard, scirrhous, fibrous, or chronic carcinomata. 

(c) Soft, medullary, encephaloid or acute carcinomata. 

(d) Carcinoma simplex, or simple cancer. 

Epithelioma 

Epithelioma is found in the skin and squamous mucous mem- 
branes, especially the lip. nose, tongue, esophagus, pharynx and 
cervix uteri. It is apt to develop where different types of epi- 
thelium join. 

Gross Pathology. — Irregular, hard, wart-like, immovable ele- 
vations are seen, which tend to ulcerate, exuding a sanious fluid. 
On section they are firm and comparatively bloodless. 

Pathologic Histology. — Irregular, branching columns of squa- 
mous cells are seen, though pressure may alter their shape, ex- 
tending from the papillae down into the deeper tissues. In normal 
skin the cells spring from the rete malpighii, and become flat- 
tened and horny as they proceed outward, but in the tumor 
instead of growing outward toward a free surface, they are 
packed in more or less rounded masses, the older cells being 
forced to the center and becoming cornined, thus forming the 
concentric whorls or "epithelial pearls" so characteristic of 
epitheliomata. Often these pearls are large enough to be visible 
to the naked eye. (Pearls are also occasionally seen in papillo- 
ma ta. ulcerative processes and in granulation tissues around in- 
growing nails.) The stroma is usually well marked, consisting 
of fibrous tissue. 



142 



GENERAL PATHOLOGY 



Growth is usually slow and sometimes latent for years; while 
malignant, epitheliomata are less so than glandular carcinomata, 
and metastasis may not occur for years, but in rare instances 
has occurred in the first year. (Fig. 50.) 

Rodent ulcer is an epithelioma occurring upon the upper part 
of the cheek. Its cells are polygonal or even spindle-shaped in- 
stead of squamous, and are arranged in anastomosing columns. 
Pearls are not found. 

These and other growths of like structure have been called 




Fig. 50.— Squamous epithelioma, a, epithelial masses; b, epithelial pearls; c, connective 
tissue; d, capillary hlood vessels. (McFarland.) 

basal cell carcinomata, because the cells retain their resemblance 
to those of the basal layer of the rete malpighii from which they 
are derived, whereas in the more slowly growing skin cancers 
the cells become flat and squamous in appearance. 

The molhiscum contagiosum is a small, soft epithelioma, found 
oftenest on the face, arms, chest and external genitals, and usu- 
ally multiple. It consists of radial, hyperplastic columns of the 



TUMORS 143 

rete malpighii, with degenerated cells in the center, which usu- 
ally show granular bodies, believed by some to be parasites. 

Adenocarcinomata 

Adenocarcinoma, or "malignant adenoma," is a carcinoma 
resembling the glandular tissue from which it springs. This 
tumor arises primarily from the mucous membranes, especially 
of the stomach, rectum, uterus, oviducts, gall bladder and bile 
ducts. It is secondary in the liver, lymph glands, lungs, kidneys, 
and bones. These tumors are more apt to occur in the young than 
the epitheliomata. 

Gross Pathology. — Adenocarcinomata are usually soft and on 
section appear gelatinous; there is a tendency to infiltrate and 
to grow outwardly into polypoid masses. (Fig. 51.) 

Pathologic Histology. — Irregular tubular alveoli are seen, lined 
with columnar cells in one or more layers, the outer layers being 
the more typically columnar. The alveoli are separated by fibrous 
or mucoid stroma. In later stages the alveoli are filled with 
various-shaped epithelial cells and the tubular character may be 
lost. In typical cases the alveoli are not solidly filled with cells 
(at least all the alveoli are not so filled) thus distinguishing these 
tumors from the scirrhous and medullary forms. 

Malignancy. — Adenocarcinomata usually grow rapidly, and 
metastasis occurs early. 

Scirrhous Carcinoma 

Scirrhous carcinoma is a hard, fibrous tumor found most fre- 
quently in the breast (female), uterus, pylorus, esophagus, rec- 
tum, and kidney. 

Gross Pathology. — Scirrhous cancer is a hard, round or irregu- 
lar tumor adherent to the overlying skin and adjacent tissues, ex- 
cept in very early stages. By contraction of the fibrous stroma, 
in the breasts, it causes retraction of the nipple, and irregulari- 
ties of the surface. Section shows a grayish white, glistening 
surface, the central part of which may retract. Yellow areas 
of fatty tissue are often seen in the center of the tumor. It is 
not encapsulated, the periphery being the more vascular part of 
the growth. Sometimes contraction is more rapid than prolifera- 
tion, causing the atrophic scirrhous cancer. (Fig. 52.) 



144 



GENERAL PATHOLOGY 




Fig. 51. — Adenocarcinoma of the body of the uterus, o, may be likened to a main 
stem from which arise numerous secondary stems, which in turn give off delicate ter- 
minals, consisting of epithelial cells. The glands may be divided into groups a, b, c, d, and 
c, by the stems of stroma f, g, and h. The stems are covered by several layers of cylin- 
dric epithelium, while projecting into the gland cavities are long slender ingrowths of 
epithelium, devoid of stroma, as seen in i. Very delicate ingrowths consisting merely of 
two layers of epithelium are seen at k and k. At / the epithelium is several layers in 
thickness, and at m many layers with leucocytes. The arborescent character of the growth 
and peculiar gland grouping are characteristic of adenocarcinoma. (Cullen.) 



TUMORS 145 

Pathologic Histology.— Conspicuous bands of fibrous tissue 
form alveoli, enclosing nests of epithelial cells. The blood ves- 
sels are thick and fibrous. The alveoli in the center of the tumor 
are smaller than toward the periphery, and the cells are atrophied 
or variously degenerated. 

Secondary involvement of the lymphatic glands occurs within 
the first year. 

Medullary Carcinoma 

Medullary carcinoma is a soft, rapidly growing, brain-like 
tumor, found most frequently in the mammae and testes. Secon- 







m% 










- a*.. 







Fig. 52. — Scirrhous carcinoma of breast. Alveoli of epithelial cells small; stroma abun- 
dant. (Mallory.) 

dary tumors of this type may follow the scirrhous form. Medul- 
lary cancer occurs somewhat earlier in life than scirrhous, but 
is much less common than the latter. 

Gross Pathology. — This tumor is soft and sometimes fluctuat- 
ing, nodular in outline, and tending to ulcerate and bleed (fungus 
hematodes). The skin adheres early and retracts, but there is 
no retraction of the nipple when the breast is involved. The 
tumor is fairly well circumscribed owing to its rapid growth. 
(Fig. 53.) 



146 GENERAL PATHOLOGY 

Pathologic Histology. — The fibrous stroma is more or less em- 
bryonic, vascular and scant. The alveoli are large and filled 
with epithelial cells proliferating rapidly, sometimes showing 
mitosis. 

These tumors are usually rapidly fatal. 

Carcinoma simplex is a form intermediate between the scir- 
rhous and the medullary forms in the relative proportion of 
stroma, cells, and vascularity. 

Melanocarcinoma is very rare, but occurs in the skin; is soft 
and malignant. 

Adamantinoma is rare, occurring on the surfaces or within 




Fig. 53. — Medullary carcinoma of breast. (Stengel and Fox.) 

the substance of the jaw bone. It appears to be derived from 
the enamel of developing teeth, and consists of a fibrillar stroma 
surrounding irregular masses of epithelial cells. It is usually 
benign, but may infiltrate and cause atrophy of the jaw, and some- 
times become sarcomatous. 

Endotheliomata 

Endotheliomata are tumors derived from endothelium of blood 
and lymphatic vessels, also the mesothelium of serous membranes, 
and hence are called hemangio endotheliomata, hjmpliangioenelo- 
theliomata, peritheliomata (from the perivascular lymph spaces) 
and mesothcliomata. 



TUMORS 



147 



In addition to the general locations mentioned, they occur in 
the meninges, periosteum, bone marrow and other parts. While 
normal endothelial cells are elongated and thin, ''forming a mo- 
saic over the surfaces which they line," in the new growths the 
cells become cuboidal, cylindrical, and irregular in shape. They 
may occur in tubular masses, or in several layers with an open 
lumen here and there, or in solid alveolar masses resembling 
carcinoma. (Fig. 54.) 

A psammoma is usually an endothelioma, occurring in the 
meninges and other parts of the brain, consisting of closely 



iilP 

amSM 




Fig. 54. — Endothelioma of the dura mater. a, connective-tissue stroma; b, small- 
celled focus; c, proliferated endothelium from lymph vessels; d, endothelial strand with 
lumen; e, area of fatty degeneration; /, endothelial cells passing into the connective tis- 
sue on the right. (Ziegler.) 



packed concentric masses of cells or whorls. They contain gran- 
ules of calcareous matter ("brain sand") . Any type of tumor how- 
ever in these locations containing calcareous granules is called 
a psammoma. 

The stroma of endotheliomata may become hyaline, myxoma- 
tous, fibrous or cartilaginous, or may atrophy, leaving the en- 
dothelium and blood vessels as the main features. Such tumors 
in which hyaline or mucoid material occurs in cylindrical masses 
are often called cylindromata. 

Endotheliomata are usually benign. 



148 GENERAL PATHOLOGY 

Teratomata 

Teratomata are tumors of complex or mixed tissues, occurring 
in abnormal locations, and due to developmental misplacements 
of tissues. 

They are said to be endogenous, when superficial tissues have 
been ''included" within internal parts, and ectogenous, when a 
part of one fetus has been included within another fetus, thus 
forming the point of origin of subsequent tumor formation. In 
this form there are all variations and amounts of inclusions up 
to double monsters. 

Dermoid Cysts 

Dermoid cysts are teratoid tumors, characterized by the pres- 
ence of skin or one or more of its appendages, as hair, nails, teeth, 
etc. They may be congenital or begin to form late in life. 

Seats. — Dermoid cysts are most frequent in the ovary, but also 
occur in the testicle and other organs. They are apt to develop 
at the junction of fetal clefts and fissures, as the orbital and 
mandibular fissures, branchial clefts, etc. 

Gross Pathology. — The growths are solid, but later become 
cystic by retention of sebaceous matter, sweat, etc., which gives 
them a putty-like consistence. They are round, smooth tumors, 
varying in size up to that of a child's head. 

Microscopically, tissues of the three blastodermic layers are 
present. Skin appears in patches over the inner surface of the 
cyst, with a great preponderance of sebaceous glands. Parts 
not covered by skin are usually covered by mucous membrane 
and glands. Besides the skin appendages, spicules of bone, mus- 
cle, nerve and brain tissue may be seen. 

The tumor is usually benign, but may become carcinomatous. 

Hypernephroma 

Hypernephroma, or Grawitz's tumor, springs from a portion of 
the suprarenal cortex included within the kidney. The tumor is 
a yellow new growth appearang under the renal capsule in the 
upper portion of this organ. It is usually small, but may be- 
come large. Histologically there are found epithelial cells ar- 
ranged in tubules as in the cortex of the suprarenal capsules. 



TUMORS 



149 



No medullary cells are present, hence no secretion of epinephrine 
has been found. (Fig. 55.) 

Cholesteatoma is a tumor exhibiting whitish glistening bodies 
of concentric layers of epithelioid cells. These bodies often con- 
tain crystals of cholesterin. The tumor occurs in the brain and 
meninges and is often multiple. Hairs, hair follicles, and horny 
changes have been found in these tumors, which places them 
among the teratomata. 

Chorionepithelioma, or syncytioma malignum, is a rapidly 
growing tumor, springing from the placental area during preg- 



IKS .>.*** t *c$ 



■f 



'& 



>3Ji* 










Fig. 55. — Finer structure of the adenomatous form of hypernephroma. (After Stengel 

and Fox ) 

nancy or the puerperium. The tissue resembles placental tissue. 
The uterine Avail is rapidly invaded and metastasis occurs to 
lungs and rarely elsewhere. The tumor has no blood vessels but 
grows within the placental spaces. (Fig. 56.) 

Cysts 

Cysts are abnormal collections of fluid or semifluid materials 
within a closed, sac-like cavity. 

They are usually classified and named as follows: 
1. Retention Cysts. — These are due to occlusion of the excre- 
tory ducts of a gland, causing distention with accumulating se- 



150 GENERAL PATHOLOGY 

cretions, e.g., wens, or sebaceous gland cysts; ranulce, from the 
salivary or mucous glands in the floor of the mouth; also renal, 
ovarian, parovarian, mammary and pancreatic cysts. An entire 
organ may become cystic, as the kidney in hydronephrosis (from 
an occluded ureter). (Fig. 57.) 

2. Softening or Necrotic Cysts. — These are due to degeneration 
and liquefaction necrosis of normal or pathologic tissues, and 
condensation of the surrounding tissue into a limiting area or 










/ 



Fig. 56. — Chorionepithelioma or syncytioma malignum. (By the courtesy of Dr. Barton 
Cooke Hirst from a painting made for him from a slide belonging to Dr. Herbert Fox.) 

wall. They occur frequently in tumors, infarcts, etc., and may 
follow hemorrhages {hemorrhagic cysts). 

3. Parasitic Cysts. — Necrotic softening occurs, irritation causes 
the formation of a capsule, and the liquid contents contain epi- 
thelial debris and parasites. Such are the hydatid cysts, due to 
the tenia echinococcus, occurring usually in the liver, less often else- 
where ; also cysts of the trichina spiralis, usually of small size, 
just visible to the naked eye, and occurring within the muscle 
tissues. 

4. Glandular Cysts, or Cystomata. — These are adenomata, 
which tend to cyst formation. They occur usually in the ovary 



TUMORS 



151 



and testicle, but may be found in any glandular tissue. They 
may be single or multiple, and each, may consist of one or many 
cavities (multilocular cysts). They vary in size up to that of a 
child's head or larger. On section a more or less serous, some- 
times hemorrhagic fluid, or a gelatinous material (usually re- 
ferred to as "colloid") may be seen. The inner surface may 




Fig. 57.- — Cyst of the parovarium: there is no distortion of the ovary; the Fallopian tube 
has been much elongated. 



be smooth, or present papillomatous outgrowths (papuliferous 
cysts or cystomata). 

Microscopically, the cysts are lined with typical, or variously 
modified, columnar epithelium, supported upon a framework of 
connective tissue. The latter may greatly predominate, causing 
the cysts to be very small, or the acini few; again the opposite 
may be true. 

Cysts are benign, though some have a tendency to become car- 
cinomatous. 



CHAPTER VIII 

THE PATHOLOGY OF INFECTIOUS DISEASES 

An Infectious Disease is one that is caused, by living micro- 
organisms. A Contagious Disease is an infectious disease that is 
readily transmitted from one individual to another by direct 
contact, by fomites, etc. 

Any organism that lives upon or within the living tissues of 
plant or animal is called a parasite. An organism which lives 
upon dead and decomposing organic matter is called a sapropliyte. 
Those parasites or saprophytes which can live and nourish in either 
condition are known as facultative or optional parasites or sa- 
prophytes. All pathogenic microorganisms are parasitic; some 
are habitual parasites, as certain pyococci, the B. coli communis, 
etc., while other, as the B. tetani, are but temporarily parasitic. 
All pathogenic parasites, which can be grown upon artificial 
culture media, are facultative saprophytes. 

The organisms pathogenic for man may be classified as fol- 
lows : 

Bacteria, or Schizomycetes (fission fungi). 

Yeasts, or Blastomycetes (budding fungi). 

Molds, or Hyphomycetes (thread fungi). 

Protozoa, or unicellular animal microorganisms. 

Metazoa, or multicellular animal organisms. 

It is customary to refer to a disease caused by bacteria or 
protozoa as an infection; to one caused by yeasts as a blastomy- 
cosis; to one caused by molds as a mycosis; and to one due to 
metazoa as an infestation. 

Bacteria are unicellular, vegetable 1 microorganisms, which re- 



1 The question whether bacteria belong to the vegetable or animal kingdom is still 
an open one. They are considered plants by most biologists because many bacteria can 
be made to grow upon inorganic food, and because in growth and reproduction they 
resemble plants more closely than animals. Bacteria, however, are such primitive forms 
and so slightly differentiated, resembling plants in rigidity of form, in tendency to 
filamentous growth and ability of some of them to grow on inorganic food, and on 
the other hand resembling animals in motility, lack of chlorophyl and apparent neces- 
sity of some for organic food, that they are generally regarded as occupying a place 
intermediate between the plant and the animal. In 1878 Haeckel proposed that bac- 
teria be placed in a separate kingdom to be known as Protista, but this suggestion was 
never generally accepted. 

152 



PATHOLOGY OF INFECTIOUS DISEASES 153 

produce by fission. Elongated bacteria (bacilli and spirilla) di- 
vide transversely, thus differentiating them from protozoa which 
divide longitudinally. 

Bacteria are divided into (a) Lower Bacteria (Haplobacteria) — 
each individual organism of which is composed of a single cell, 
capable of performing all the vital essential functions and (b) 
Higher Bacteria (Trichobacteria, or Trichomycetes) — composed 
of filamentous forms (thread-like arrangement of cells) with real 
or apparent branchings. The end-cells only appear to reproduce, 
hence there is here the beginning of a division of physiologic 
function. 

Bacteria cause disease mainly by the production of specific 
toxins; i.e., poisonous substances secreted by the bacteria, and 
peculiar (hence "specific") to the particular organism which se- 
cretes them. Toxins resemble enzymes in all essential properties, 
and are usually divided into (a) true, soluble or extracellular 
toxins, — toxins which in culture media escape from the bacterial 
cell (extracellular) and diffuse through the medium (soluble), 
and (b) intracellular, endotoxins, such as the toxins of pyococci, 
the typhoid bacillus and most of the pathogenic bacteria — toxins 
which remain within the bacterial cells (intracellular) and are 
liberated in disease when the bacterial cells disintegrate. In 
addition to the specific toxins, bacteria may also form various 
other metabolic products, such as hemolysins, coagulating, pro- 
teolytic and other ferments, as well as various nonspecific and 
specific substances. 

When bacteria with their toxic products gain entrance into 
the blood and tissues, the}' stimulate the tissue cells to the pro- 
duction of defensive substances, or antibodies. All cells or sub- 
stances capable of causing living tissues to form antibodies are 
called antigens. The most important antibodies are antitoxins, 
which combine with and neutralize toxins, thus rendering the latter 
harmless; agglutinins, which cause bacteria to clump together; 
lysins, which destroy bacteria and other cells; and opsonins, which 
prepare bacteria in some manner so that they are more easily 
ingested and destroyed by the phagocj^tic leucocytes. 

Immunity is a state of resistance to an infection. It may be 
actively acquired by the production of antibodies during the 
course of an infection, or during the process of intentional in- 



154 GENERAL PATHOLOGY 

oculation, as in "immunization" in which animals are inoculated 
for the purpose of producing antitoxic and bacteriolytic sera, or 
as in "vaccination" or " bacterination, " in which attenuated or 
killed cultures of bacteria are inoculated into healthy persons to 
cause the formation of antibodies as a matter of protection against 
infection, or into diseased individuals for the purpose of effect- 
ing a cure of the disease. Immunity may also be passively ac- 
quired when antitoxic sera ("antitoxins") and bacteriolytic sera 
("antisera"), manufactured within the tissues of an animal or 
even a human being, are injected into the tissues of another in- 
dividual for the purpose of protection or cure. 

Natural immunity is not well understood, but may be defined 
as that which is possessed by an individual or race, not known 
to have experienced any of the recognized processes of protec- 
tion. 

A septicemia (or bacteremia) is a disease due to the presence 
of bacteria with their toxins in the blood. Thus typhoid fever, 
anthrax, etc., are septicemias, as well as generalized staphylococ- 
cic or streptococcic infection, though surgeons are apt to limit the 
term "septicemia" to invasion of the blood by pyogenic organ- 
isms. 

A pyemia is a condition in which secondary (metastatic) ab- 
scesses appear in various organs and tissues, formed by bacterial 
emboli brought by way of the blood vessels or lymphatic vessels 
from some primary focus of suppurative inflammation. 

A toxemia is a diseased condition due to the absorption of the 
toxins of pathogenic bacteria, as in tetanus. 

A sapremia is a condition due to the absorption into the blood 
of poisonous substance formed by saprophytic bacteria growing 
in mortifying tissues, as in certain forms of gangrene, retained 
portions of placenta after parturition, etc. 

SUPPURATIVE DISEASES 

Suppuration (q.v.) or inflammation resulting in pus formation, 
when occurring naturally, is always the result of the invasion 
and activity of microorganisms. The most common pyogenic or- 
ganisms are the staphylococci and streptococci; less often the 
pneumococci, the pneumobacilli, gonococci, the colon and typhoid 
bacilli ; still less commonly, other microorganisms, including ame- 



PATHOLOGY OF INFECTIOUS DISEASES 155 

bae, may become pyogenic. Under perfectly favorable conditions 
it is believed that most, if not all, pathogenic bacteria may cause 
suppuration. 

The micrococcus tetragenus and the B. pyocyaneus are often 
associated with the more common pyococci in causing suppura- 
tion, the latter giving a green tinge to the pus, but they rarely 
if ever are the sole cause from the beginning to the end of the 
infection. 

The staphylococcus pyogenes aureus (cluster-forming, pus-pro- 
ducing golden yellow spherical organism) is the direct cause, as 
a rule, of localized and circumscribed inflammation and suppura- 
tion, such as abscesses, pustules, furuncles, carbuncles, etc. 
When these cocci gain entrance into the circulation, pyemia and 
septicemia may result, though less often than in streptococcal in- 
fection. The organisms may remain dormant at times within 
an encapsulated inactive abscess, or in deeply seated subacute 
infections, as in subacute osteomyelitis, endocarditis, etc., and 
later become active and virulent. The presence of staphylococci 
in association (symbiosis) with other organisms in disease often 
aids the activity of the latter, as for example the influenza bacilli. 

Their specific toxins are intracellular, and have a decided chemo- 
tactic effect upon the leucocytes, attracting large numbers of 
these phagocytes to the seat of infection. A hemolytic substance 
is also formed. Although staphylococci cause the formation of 
antibodies, the use of antistreptococcic sera has not been very en- 
couraging, but the use of vaccines of killed or attenuated cul- 
tures has been more promising, especially in subacute or chronic 
staphylococcic infections. 

The staphylococcus pyogenes albus, and the staphylococcus epi- 
dermidis albus are mildly pathogenic forms, probably but slightly 
modified varieties of the S. pyogenes aureus. The first is often 
associated with the aureus variety in suppurations, or may be 
the sole cause in certain forms of acne. The latter inhabits the 
layers of the epiderm, and in the opinion of some bacteriologists 
is the cause of "stitch abscesses.'' 

The Streptococcus pyogenes (chain-forming, pus-producing coc- 
cus) varies considerably in virulence, but usually causes the 
more severe forms of suppurative disease, with a tendency to 
spread and become phlegmonous. Cellulitis, erysipelas, perios- 



156 GENERAL PATHOLOGY 

titis, pleuritis, peritonitis, etc., as also general septicemia, are 
more often due to streptococci than to staphylococci. Strep- 
tococci are, however, also found in localized suppurations. In 
malignant endocarditis the Streptococcus viridans, a variety form- 
ing green colonies on culture media, is commonly found. In rheu- 
matic arthritis the Streptococcus rheumaticus is apparently the 
chief exciting cause. In erj^sipelas the Streptococcus erysipelatis 
is found, but this appears to be identical with the Streptococcus 
pyogenes. Erysipelas, (literally "red skin") is a serous inflam- 
mation of the skin, usually found on the face, tending to spread 
from the nose outward across the cheeks, and preceded by a zone 
of congestion and dense infiltration which follows the lymphatic 
clefts. Occasionally suppuration occurs. 

Streptococci are often found in the throat and tonsils during 
infectious diseases, such as measles, scarlatina, influenza, etc. 

Eosenow believes that streptococci and pneumococci are 
merely different varieties of one species and has apparently suc- 
ceeded in transmuting one to the other variety under artificial 
conditions. 

In regard to toxins, antibodies, and vaccines, what was said 
of the staphylococci is also true in general of the streptococci. 

Epidemic Cerebrospinal Meningitis 

Epidemic cerebrospinal meningitis is a purulent inflammation of 
the cerebral and spinal meninges, caused by the meningococcus, 
or Diplococcus intracellular is meningitidis. These cocci occur in 
pairs, and resemble the gonococci both in morphology and in 
being found in groups within the leucocytes and other cells. They 
also sometimes occur in chains. 

The disease is a fibrinopurulent, less often a seropurulent lep- 
tomeningitis, the cerebral dura being rarely involved, although 
the spinal dura is often involved. The exudate is abundant in 
the large fissures of the brain, over the optic chiasm and sur- 
faces of the pons and the cerebellum. The inflammation usually 
follows the blood and lymph vessels into the substance of the 
brain and cord, often resulting in small abscesses. The fluid 
from a lumbar puncture nearly always contains the cocci, and 
the cocci have frequently been found in the nasal secretions of 
patients and of persons exposed to the disease. It is believed 



PATHOLOGY OF INFECTIOUS DISEASES 157 

that meningeal invasion occurs by way of the lymphatic vessels 
from the nose. 

Various inflammations and degenerations are also noted in the 
kidneys, heart, spleen, muscles, and other tissues. 

Gonorrhea 

Gonorrhea is a purulent, catarrhal inflammation of the urethra 
and other mucous membranes, caused by the gonococcus or Mi- 
crococcus gonorrheal This organism occurs in pairs, "biscuit- 
shaped" or "coffee-bean-shaped" in appearance, and found 
abundantly in the pus of acute gonorrhea of the urethra, less 
often in chronic cases, or in other locations. In acute gonor- 
rheal urethritis the inflammation begins at the meatus and soon 
spreads to the posterior parts: the mucosa is intensely red, and 
in about twenty-four hours or more a yellowish (sometimes 
greenish) exudate appears, consisting of leucocytes and des- 
quamated epithelium. Microscopical examination shows groups 
of the gonococci lying within the pus cells, as well as in the fluid 
portion of the exudate. 

From the original focus, other tissues are readily invaded, 
causing salpingitis, oophoritis, peritonitis, prostatitis, also me- 
tastasis to more remote tissues, as the heart and the joints (gonor- 
rheal endocarditis and arthritis). "Gonorrheal rheumatism" 
usually occurs months after the infection, is very intractable and 
apt to result in permanent damage to the joint, usually the knee, 
elbow or wrist. 

Ophthalmia neonatorum is an acute gonorrheal conjunctivitis 
contracted by the child from the mother during parturition. It 
is said that 10 per cent of blindness in children is due to this 
form of gonorrhea. 

Chronic gonorrhea is usually a direct continuation of an acute 
attack, and characterized by a constant discharge of a thin, 
catarrhal exudate (gleet). Ulcerous lesions, or papillomatous 
thickenings of the mucosa are a frequent result of chronic gonor- 
rhea, or there may be hyperplasia of the submucosal connective 
tissue with narrowing of the urethra (stricture). The most com- 
mon seat of stricture is the membranous urethra. 



158 



GENERAL PATHOLOGY 



The gonotoxin is intracellular, and while slight amounts of 
antibodies are produced, antisera are valueless, but vaccines may 
be useful in chronic forms of the disease. 

While gonorrhea is usually contracted through sexual contact, 
the transmission of the disease by towels, bedding, and other 
contaminated articles, particularly in institutions, is probably 
more frequent that is generally recognized. Latent gonorrheal 
foci, existing long periods of time after apparent "cures" have 
been effected, and capable of becoming acute and transmitting 









¥Js 





Fig. 58. — Acute urethritis, showing purulent infiltration and gonococci in the cells and 
between the cells. (Birch-llirschfeld.) 

the disease to others, are also more frequent than is generally 
believed. (Fig. 58.) 



Soft Chancre, or Chancroid 

Soft chancre, or chancroid, is an ulcer almost invariably found 
on the external genitals, due to the B. of Dticrey. It is always 
contracted through sexual contact, but is autoinoculable, hence 
there are usually more than one ulcer. The infection begins as a 
red papule, which later suppurates, forming a yellowish ulcer 
with irregular infiltrated margins. Sometimes it becomes phage- 



PATHOLOGY OF INFECTIOUS DISEASES 159 

denic or serpiginous in character. The organisms travel along 
the lymphatic channels to the inguinal glands which also sup- 
purate as a rule. The disease is purely local — never systemic 
when uncomplicated. Mixed infection often occurs, and gono- 
cocci, Spirochete pallida, pyogenic cocci, and other organisms may 
be found in the ulcers. 

Pneumonia, or Pneumonitis 

Pneumonia is an inflammation of the essential lung tissue ; viz., 
the alveoli and their immediately surrounding structures. The 
clinical forms of pneumonia are practically always due to micro- 
organisms, but many different species of the latter have been 
found as the direct cause of the disease, and it is possible, more- 
over, to produce a pneumonia by the inhalation of hot steam 
or chemical irritants. Pneumonia, therefore, should be con- 
sidered as a distinct pathologic condition rather than a specific 
infection. Classified according to their pathologic anatomy, pneu- 
monias may be divided into: 

Lobar, Fibrinous or Croupous Pneumonia. 
Lobular, Catarrhal or Bronchopneumonia. 
Purulent or Suppurative Pneumonia. 
Fibroid, Interstitial or Productive Pneumonia. 
Tuberculous or Caseous Pneumonia. 

Lobar, or Croupous, Pneumonia is an acute hemorrhagic and 
exudative inflammation of the air cells of one or more lobes of 
the lungs, due usually to the pncumococcus, or Biplococcus pneu- 
moniae, but occasionally to streptococci, staphylococci, B. influ- 
enzae, the B. of Friedlander, and other organisms, either alone 
or in association (symbiosis) with the pneumococcus. 

Cold, fatigue and systemic depression of any nature act as pre- 
disposing causes. The lower right lobe is of tenest affected ; next 
the lower left lobe, and rarely the apices. In "double pneu- 
monia" lobes in both sides of the thorax are simultaneously in- 
volved. 

There are three principal stages : 

(a) Congestion. — The diseased area is hyperergic, dark red, less 
crepitant than normal, heavy but still floating when placed in 
water, and the pleural surfaces are lustreless. Microscopically, 
the capillaries are congested, and the air cells contain a serous 



160 



GENERAL PATHOLOGY 



exudate with red and white blood cells, and a few desquamated 
epithelial cells. As this exudate increases in amount, coagulation 
sets in (few hours to a few days) thus forming the 

(b) Stage of Consolidation or Hepatization. — The affected area 
is now solid and liver-like, deep red or brownish red in color 
(red hepatization), is swollen, pits on pressure and sinks when 
placed in water. On section the cut surface is red, dry, and 
granular — due to plugs of fibrin projecting from the air cells. 
A fairly thick slice of the diseased lobe will break on bending. 
Microscopically the air vesicles are filled with fibrin holding in its 







Fig. 59. — Acute lobar pneumonia. Early stage. This single air vesicle shows conges- 
tion of the capillaries in the walls, and a small amount of exudates, fibrin, leucocytes, 
red blood cells, and exfoliated epithelium. (Uelafield and Prudden.) 







meshes red and white cells and desquamated epithelium. The 
fibrin soon begins to contract causing a serous fluid to collect 
in the vesicles, the red cells disintegrate, the epithelial cells be- 
come fatty, and when these changes have advanced far enough 
to give the affected areas a yellow or grayish color, the name 
"gray hepatization" is applied. The area is still solid but less 
apt to break on bending, and the air cells contain a mass of fibrin 
which is retracted from the walls and cells, chiefly leucocytes and 
epithelium. (Figs. 59 and 60.) This substage (gray hepatiza- 
tion) does not always develop — the red hepatization passing at 
once into the third stage of 

(c) Resolution. — The affected area now softens, pitting is no 



PATHOLOGY OF INFECTIOUS DISEASES 



161 



longer possible and crepitation can again be elicited. On section 
a purulent fluid exudes. 

Microscopically, liquefaction necrosis, with cells in different 
stages of disintegration are the chief features. Proliferation of 
epithelial cells becomes marked, thus repairing the damaged al- 
veolar walls, while the softened, emulsified contents are being 
absorbed by the lymphatics and in part expectorated. 

During the course of the disease, the lung tissues surrounding 
the inflamed parts are more or less emphysematous, and the pleura 
is usually inflamed, hence a typical pneumonia is nearly always a 




Fig. 60. — Acute lobar pneumonia. Later stage. The air vesicles are filled with exu- 
date consisting of leucocytes, fibrin, and serum with a few epithelium cells. (Delafield 
and Prudden.) 

pleuropneumonia. A blood examination shows leucocytosis. 
Rarely, in intense intoxications a leucopenia is present. Paren- 
chymatous changes in the kidneys and heart may occur due to 
the toxemia; albuminuria is frequent, and the chlorides are di- 
minished or absent from the urine during the disease, but usually 
reappear in excess during convalescence. 



Bronchopneumonia or Lobular Pneumonia 

Bronchopneumonia or lobular pneumonia is an acute inflamma- 
tion starting in the smaller bronchioles and extending to the air 
cells of the lungs, in which the exudate shows little or no ten- 
dency to fibrin formation. About one-half of the lobular forms 



162 



GENERAL PATHOLOGY 



of pneumonia are due to the pneumococcus, either alone or as- 
sociated with the organisms mentioned under croupous pneu- 
monia. Any of the organisms mentioned may also be the sole 
cause of this form of pneumonia. 

Bronchopneumonia is most frequent in the young and the aged, 
and may be secondary to measles, whooping cough, scarlatina, 
diphtheria, pulmonary cirrhosis, typhoid fever, etc. 

Grossly the pleural surface presents red or grayish areas, which 
correspond to the lobules or areas of the terminal bronchioles 
affected. In extensive cases all the lobes of both lungs may be 




Fig. 61. — Bronchopneumonia. Child. The wall of the small bronchus is thickened 
and the lumen contains a mucopurulent exudate. The adjacent air vesicles also con- 
tain a catarrhal exudate. (Delafield and Prudden.) 

involved, but not all the lobules are affected, i.e., the lobes are 
not uniformly affected as in lobar pneumonia. The inflamed, 
lobular areas usually project slightly above the surrounding sur- 
faces, and are surrounded by emphysematous tissue. The lung as 
a whole is crepitant, but the localized diseased areas are airless 
and sink in water. The bronchi and bronchioles contain muco- 
purulent exudates, and their complete obstruction sometimes leads 
to local areas of atelectasis. (Fig. 61.) 

Microscopically the alveoli are filled with a semifluid exudate 
containing desquamated epithelium and blood cells. The alveolar 
walls show round-cell infiltration and the bronchioles catarrhal 
bronchitis. 



PATHOLOGY OF INFECTIOUS DISEASES 163 

Hypostatic pneumonia is a bronchopneumonia, not so distinctly 
lobular as the ordinary form, and with an exudate that is more 
fibrinous. It commonly involves the bases and posterior (de- 
pendent) parts of the lungs in individuals who are confined to 
bed during prostrating diseases, as typhoid or chronic nephritis. 
When the heart action becomes feeble hypostatic congestion de- 
velops in the dependent parts and soon bacteria enter the con- 
gested part and set up a catarrhal inflammation. 

Aspiration pneumonia is also a form of bronchopneumonia re- 
sulting from the inspiration of infectious material from the upper 
air passages, as well as food and secretions from the mouth in 
cases of paralysis, in anesthesia, or from the inhalation of hot 
steam, chemical irritants or dust in concentrated form. The le- 
sions vary with the causal factors. When infectious or highly 
irritating matter is "aspirated," an intense catarrhal inflamma- 
tion with solidification results; the exudate is hemorrhagic and 
liable to become suppurative or necrotic. In the inhalation of 
dust, as in marble cutting, coal mining, etc., the catarrhal inflam- 
mation may be moderate in degree or absent, while the produc- 
tive inflammation, with a resulting fibroid pneumonia, may be the 
main pathologic change. 

Purulent pneumonia is an acute inflammation in which pyogenic 
bacteria, whether as a secondary infection brought by way of 
the bronchi, blood channels or the pleura, or as a primary in- 
fection, cause suppuration of the inflammatory exudate. Small 
miliary abscesses, or one or more large abscesses may result, a 
condition which is very apt to be fatal. When the abscesses 
break into the pleural cavity, an empyema results. The term, 
empyema, refers to a collection of pus in the pleural cavity how- 
ever produced. 

Fibroid pneumonia is a chronic process in which the cellular 
proliferation becomes permanent fibrous tissue. When this con- 
dition is caused by the inhalation of coal dust, iron dust, or 
marble dust (pneumonokoniosis) the particles penetrate the al- 
veolar walls and the walls of the bronchioles, and become sur- 
rounded by a zone of inflammatory exudate which finally or- 
ganizes into fibrous tissue. This form of pneumonia also occurs 
at times secondary to other forms of pneumonia, to syphilis, tu- 
berculosis, etc. When the indurated areas are extensive, con- 



164 GENERAL PATHOLOGY 

traction with distortion of the lung follows, with obliteration 
of the air cells and proportionate impairment of respiration. 

Caseous or tuberculous pneumonia is due to the B. tuberculosis, 
and characterized by a filling up of the air cells and an infiltration 
of the interalveolar tissues with an exudate which tends to 
caseation instead of resolution. There are small areas of con- 
solidation, usually lobular, at first red (congestion), later yellow 
(caseation). These areas finally soften and undergo resolution, 
if small, or become encapsulated, or may coalesce into larger 
cavities, resulting in chronic pulmonary tuberculosis; if mixed 
infection occurs, rapid suppurative softening results and the con- 
dition quickly becomes fatal ("galloping consumption.") 

The specific or infectious granulomata are smaller or larger 
masses of pathologic tissue, resulting from subacute or chronic 
proliferative inflammatory processes, due to specific microor- 
ganisms, and having a tendency toward degenerative or necrotic 
change. The lesions are for the most part tubercles, nodules or 
nodes, consisting essentially of more or less typical granulation 
tissue, but there is no tumor in the true sense, and the term 
"granuloma" is deservedly falling into disuse. 

The lesions usually described under this heading are those 
found in tuberculosis, leprosy, glanders, syphilis, rhinoscleroma, 
actinomycosis, sporotrichosis, blastomycosis, etc. 

In the following pages the pathology of the lower or true 
bacterial diseases will be considered immediately, while those 
morbid conditions due to the higher bacteria and other organisms 
will be taken up in their proper order. 

Tuberculosis 

Tuberculosis is a disease comprising the morbid processes due 
to the B. tuberculosis. It affects man and practically all the lower 
animals, though goats, horses, dogs, and cats are relatively im- 
mune. 

Locations. — It is found in the respiratory tract, the gastroin- 
testinal tract (especially the lower ileum, rectum, throat and 
mouth), the lymph nodes, serous membranes, bones, spleen, kid- 
neys, adrenals, brain, middle ear, uterus with appendages, tes- 
ticles, bladder, and skin. Organs which are rarely affected are 



PATHOLOGY OF INFECTIOUS DISEASES 



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165 



Fig. 62. — Miliary tubercles in the liver, showing abundant round cells in the peripheral 
parts, epithelioid and giant-cells within. (Stengel and Fox.) 




Fig. 63. — Miliary tubercle of the human form. (Stengel and Fox.) 



166 GENERAL PATHOLOGY 

the salivary glands, thyroid gland, the muscles, cartilages, ovaries 
and heart. 

In children the lymph nodes, serous membranes and the bones 
are most frequently infected. 

Gross Pathology. — The characteristic lesion is the miliary tu- 
bercle. This is a gray, semitranslucent, slightly elevated (if su- 
perficially located) nodule varying in size from a point scarcely 
visible to the naked eye to 2 mm., which merges into the sur- 
rounding tissue (can not be "peeled out"). The second form of 
tuberculous lesion is an infiltration of the tissues with epithelioid 
cells and other cells characteristic of the tuberculous process, but 
without forming distinct tubercles. When caseation sets in, the 
lesions become yellow (yellow miliary tubercle). (Figs. 62 and 
63.) 

Minute Anatomy. — The bacilli (or their toxins) first cause pro- 
liferation of the endothelial cells of the lymph spaces, lymph 
capillaries and blood vessels and connective tissue of the part. 
These cells are large . and have vesicular, poorly staining nuclei, 
and known as epithelioid cells. Giant cells (large multinucleated 
cells) may appear in the midst of the epithelioid cells, probably 
formed from the latter by proliferation of the nuclei without di- 
vision of the cytoplasm. Round cells, consisting of leucocytes 
and lymphocytes, surround the collection of epithelioid cells, and 
at this stage it may be possible at times to see the three zones 
usually described as consisting of an inner zone of giant cells, 
a middle zone of epithelioid cells and an outer zone of round 
cells. This is the histology of the gray tubercle ; no new blood 
vessels are formed, and after a variable time, the center becomes 
cheesy (cheesy necrosis), the cells lose their outline and the 
nuclei degenerate, giving the field a granular appearance, which, 
surrounded by cells not yet having undergone degeneration, 
presents the so-called "raked field" appearance. The giant cells 
also degenerate, and those which have undergone but partial 
degeneration have a crescentic outline. Giant cells are not neces- 
sarily present, but are characteristic of a typical tubercle. 

The histologic appearance of tuberculous infiltration is essen- 
tially the same, but there are more blood vessels in the area, and 
especially upon free surfaces a typical, highly vascular granula- 
tion tissue may be formed. 



PATHOLOGY OF INFECTIOUS DISEASES 167 

Results. — When well established, the disease progresses usu- 
ally to a fatal termination. Many times, however, caseation may 
be followed by encapsulation with temporary arrest of the in- 
fectious process (latent foci), or by calcification, and if the dis- 
ease has not progressed too far, a permanent cure is possible. 
When the lesions undergo liquefaction, cavities (vomicae) are 
formed, or, especially in cases of bone infection, cold abscesses 
result. 

Secondary tuberculosis may be set up in various parts of the 
body by (1) extension along lymphatic channels, (2) along nat- 
ural channels, as the respiratory or intestinal tract, and (3) 
through the blood vessels. 

Leprosy 

Leprosy is a chronic infectious disease due to the B. lepra?. 

It occurs in two forms, the nodular (or tubercular) and the 
anesthetic. In the first, gray or yellowish nodules develop, vary- 
ing in size up to a walnut, or larger. (Fig. 64.) These occur in 
the skin and subcutaneous tissues of the face, exterior surfaces 
of the legs and arms, about the hands and other parts, and are 
red and inflammatory at first, but later pale and indolent. They 
usually break down into ulcers which slowly cicatrize, often with 
great distortion. The mucous membrane and internal organs may 
also rarely be affected. 

In the anesthetic form the lesions are less conspicuous, but the 
hyperesthesia, neuralgia and later atrophic ulcers make it more 
serious than the nodular form. Anesthesia of the parts occurs 
when the ulcerations develop. 

The two forms are often associated, and tuberculosis often fol- 
lows the lesions, especially those of the internal organs. 

Microscopically, the nodule is seen to be fibrous, somewhat vas- 
cular without tendency toward caseation. It is composed of 
epithelioid cells (proliferated endothelium and connective tissue 
cells) which are often vacuolated and may contain the bacilli; 
large degenerated cells ("lepra cells") containing many bacilli 
and a few more or less degenerated nuclei are always found. 
Giant cells are sometimes present, but far less often than in tu- 
berculosis. 



168 



GENERAL PATHOLOGY 



In the anesthetic form the bacilli grow within the sheaths of 
nerves, forming fusiform swellings, resembling the nodules in 
structure. 

Skin eruptions (pemphigus leprosa) often occur, also atrophy 
of the parts affected, and sometimes even loss of parts, as fingers 
or toes. 




Fig. 64. — Nodular leprosy. (Goldschmidt.) 



Syphilis, or Lues (or "Great Pox") 

Syphilis is an infectious disease due to the presence of the 
Spirochete pallida, or Treponema pallidum. 2 It occurs in three 



stages. 



2 There is a tendency to place this organism among the protozoa. It is a rigid spiral, in 
many respects resembling the spirilla, but it is claimed by some observers that in 
reproduction longitudinal division takes place, which would place the spirochete among 
the animal organisms. According to Jordan (General Bacteriology, 1918), "At present the 
systematic position of this organism may be regarded as unsettled, although the majority 
of investigators incline to place it with the true bacteria, or at best in a group midway 
between the bacteria and protozoa.'' 



PATHOLOGY OF INFECTIOUS DISEASES 169 

The primary stage is characterized by the chancre, which appears 
after an incnbation period of three weeks, at the site of inocu- 
lation, as a red papule increasing in size and hardness (Hunte- 
rian chancre). It usually presents a dry, sometimes slimy super- 
ficial erosion, but does not ulcerate; is located usually upon the 
glans penis, prepuce, or just within the meatus; in the female, in 
the vagina, urethra or cervix uteri. Extragenital chancres may 
occur in the rectum, about the anus, in the mouth, eyes, groin 
and other locations. 

Wherever the initial lesion occurs, local lymphadenitis devel- 
ops simultaneously, forming the "indolent bubo" — painless, 
hard and movable beneath the skin. 

Histologically, the chancre consists of round cell infiltration 
(leucocytes and proliferated connective tissue cells) within the 
deeper layers of the skin or mucous membrane, and especially 
along the course of the blood vessels. There is considerable in- 
tercellular exudate, which coagulates, favoring necrosis of the 
superficial cells (erosion). 

The chancre attains a maximum size in one to two Aveeks, from 
a few millimeters to a few centimeters in diameter, remains sta- 
tionary for three or four weeks, then slowly disappears, though 
the induration may persist for years. 

The secondary stage may follow in about six weeks, and is 
characterized by eruptions upon the skin and mucous mem- 
branes, with swelling and induration of the lymphatic glands 
Generally. The eruptions begin as papules or macules which be- 
come flat tabular swellings with superficial erosion, having a dull 
red or coppery color on the skin, and a grayish color on the mu- 
cous membrane (the mucous patch). These eruptions are poly- 
morphous in outline, are covered with a scant secretion, often 
offensive, sensitive to the touch, and the most contagious of 
syphilitic lesions. 

Histologically, there is round cell infiltration, with edema and 
necrosis of the epithelium. The papilla become abnormally large 
and hyperemic. 

These eruptions last from one to three years, then disappear, 
and recovery may be effected, or the tertiary stage may follow. 

The tertiary stage may follow the secondary in from one to four 
years, or after many years, and is characterized by the presence 



170 GENERAL PATHOLOGY 

of guinmata, which are nodules varying in size from a pinhead to 
an orange. They occur most frequently in bones, especially tibia, 
sternum and skull; in internal organs, as liver, kidneys, lungs, 
brain and other parts. 

Macroscopically, a gumma is a hard, somewhat elastic nodule; 
on section the central part is found to be gelatinous in appearance. 
Fibrous bands are usually seen radiating from the center to the 
periphery and into the surrounding tissues. The hard and elastic 
character suggested the name "gumma," i.e., gummy tumor. The 
center may soften, especially when near a surface, forming ulcers 
which finally cicatrize. (Fig. 65.) 



Fig. 65.- —Gummatous meningoencephalitis. (Ziegler.) 

Histologically, the gumma is composed of round and spindle 
cells and usually a few giant cells. The blood vessels are markedly 
thickened, and new vessels are formed. Degeneration or a form 
of necrosis (resembling caseation) is always seen in the center of 
the gumma. 

There are also diffuse tertiary syphilitic lesions, such as bands 
of connective tissue, greatly thickened, atheromatous vessel walls, 
with a diffuse infiltration of tissues with the characteristic round 
cells; often seen in the liver, spleen, kidney, heart, and nervous 
system. 



PATHOLOGY OF INFECTIOUS DISEASES 171 

Glanders, or Equinia 

Glanders is an acute or chronic infectious disease, occurring 
spontaneously in horses, due to the B. mallei, and occasionally 
communicated to man and other animals. 

In horses, the nasal mucosa is the usual seat of inoculation, in 
which slightly elevated, pea-sized nodules appear, which increase 
and finally break down, leaving yellowish ragged-edged, pus-dis- 
charging ulcers. When these heal, characteristic, stellate scars 
are formed. Bronchopneumonia by aspiration of infected mate- 
rials from the nose or upper air passages may follow. Metastatic 
abscesses of internal organs often occur. The disease is often fatal, 
death occurring with all the symptoms of a septicemia. 

When the skin is particularly involved, the condition is called 
farcy and the nodules in the skin and subcutaneous tissues, vary- 
ing in size up to hazelnuts, are called farcy buds. These also 
tend to suppurate. Farcy is more frequently chronic in its course 
than is the nasal form, or glanders proper. 

In man, the lesions are essentially similar to those occurring in 
the horse, but the disease is usually an acute, febrile, septicemic 
affection and usually fatal, though in the rarer chronic form, 50 
per cent are said to recover. Infection occurs through the nose, 
conjunctiva, and abrasions of the skin. 

Histologically, the nodules consist of dense masses of small 
round cells of lymphoid type together with leucocytes and epi- 
thelioid cells at the periphery. When suppuration occurs these 
cells degenerate and become pus cells. Chronic glanders (rare 
in man) is characterized by slowly extending ulcers with scar 
formation. 

Rhinoscleroma (literally, a hard tumor of the nose) is a 
chronic infectious disease, characterized by the formation of 
small, hard nodules in the skin of the anterior nares and upper 
lip, with a tendency to spread over the face or into mouth and 
pharynx, observed most frequently in Europe, rarely elsewhere, 
and due to the B. rhino scleromatis, a bacillus practically identical 
in morphology and cultural characteristics with B. of Friedlander 
(pneumobacillus) . 



172 GENERAL PATHOLOGY 

THE TOXEMIC DISEASES 

All pathogenic microorganisms form toxins, but a few, such as 
the B. tetani, the B. diphtherise and the spirillum of Asiatic chol- 
era form true, soluble toxins, which are so highly poisonous, that 
these organisms may be regarded as preeminently toxicogenic, 
and the diseases produced as true toxemias. 

Tetanus or Lock Jaw- 
Tetanus is an infectious disease characterized by an intense in- 
toxication, due to the B. tetani. 

The tetanus bacillus is a spore-forming, anaerobic organism. 
It will not grow in presence of air in culture media or in the tis- 
sues. Infection therefore occurs usually through deeply pene- 
trating wounds, or when aerobic organisms are carried into 
the wound together with the tetanus bacillus or its spores, or 
when there is considerable injury to the tissues. Such conditions 
favor the anaerobic requirements of the bacillus ; wounds which 
do not fulfill these conditions are not apt to develop the infection 
even when inoculated. The tetanus bacillus is a saprophyte in 
the soil, particularly garden earth, manure, and dust, and a para- 
site in the intestines of herbivorous animals. 

The local reaction of the bacillus, apart from the inflammation 
caused by associated organisms, is usually very insignificant. 
After an incubation period of nine days (few days to several 
weeks) stiffness of the jaw and neck, or spasms of the muscles 
about the infected wound develop. Tonic spasms of these parts 
soon folloAv, and later general tonic and clonic convulsions 
develop and continue until death results from exhaustion or as- 
phyxia (spasm of the glottis), or until recovery takes place. 
These symptoms are all due to irritation of the motor cells of the 
cord and brain by the toxin, which travels along the nerve tracts 
from the infected wound to the central nervous system. 

Antitetanic serum (antitoxin) is curative, but must be used in 
time to combine with the toxin before the latter has reached the 
motor cells. Since the first symptoms are usually evident only 
when the toxin has readied the cord, the use of the serum fre- 
quently fails. Its most successful use is that of a preventive in 
cases where inoculation was thought probable. 



PATHOLOGY OF INFECTIOUS DISEASES 173 

Diphtheria 

Diphtheria is an acute infectious inflammation clue to B. cliph- 
theriae (Klebs-Loeffler bacillus), and characterized by the forma- 
tion of a false membrane locally, and by toxemia systemically. 

While the tonsils, pharynx and the nose are the common seats of 
the disease, the eyes, skin, middle ear, vagina, and other parts may 
also become infected. Symbiosis with streptococci increases the 
virulence of the diphtheritic bacillus. After an incubation of from 
2 to 7 days, an acute fibrinous inflammation sets in, the exudate of 
which as it appears upon the surface undergoes coagulation necro- 
sis, thus forming a thick, adherent membrane — the false or diph- 
theritic membrane. In the larynx this membrane with the swollen 
and inflamed mucosa may cause fatal asphyxia, but aside from this 
purely mechanical condition, diphtheria becomes serious or fatal 
only through the toxin which is formed. The bacilli rarely invade 
the blood or internal organs. At necropsy are found degeneration 
and inflammation of the myocardium and endocardium, and ne- 
phritis. Bronchopneumonia is present in over 50 per cent of fatal 
cases, due to B. diphtheriae, to pnenmococci or other organisms. 

During convalescence paralysis of the soft palate and other mus- 
cles often occurs. 

The use of antidiphtheritic serum (antitoxin) affords the best 
example of successful serotherapy in the art of therapeutics. 

Asiatic Cholera 

Asiatic cholera is an acute infectious disease characterized by 
a serous inflammation of the intestines and due to the Spirillum 
or Vibrio cliolcrac asiaticae, often called the "comma bacillus" of 
Koch. 

The spirilla invade the mucosa of the lower part of the ileum 
chiefly, also often the large bowel, causing an intense watery exuda- 
tion, which with the contained particles of desquamated epithelium, 
constitutes the "rice-water" discharges, so prominent a symptom 
of this disease. Postmortem examination reveals no definite or 
constant morbid changes, but often congestion or inflammation are 
noted in the affected parts, with degenerative changes in the liver, 
kidneys, and other organs. The spirilla do not enter the blood, 
but secrete a soluble toxin, which either alone or together with other 
toxic products accounts for the synrptonis. 



174 GENERAL PATHOLOGY 

m 

Typhoid Fever 

Typhoid fever is an acute general infection of the lymphade- 
noid tissue of the body, with its most characteristic lesions in the 
lymphoid structures of the intestine, and due to B. typhosus (B. 
typhi dbdominalis) of Eberth. The bacilli appear in the blood (a 
bouillon culture inoculated with blood during the first week of the 
disease is the most positive means of diagnosis) and in all the se- 
cretions and excretions, as well as in the "rose spots" which oc- 
cur upon the exterior early in the infection. 

As in Asiatic cholera, the organisms are usually ingested with 
food and water. After an incubation period of two or three 
weeks, the solitary follicles and Peyer's patches in the lower 
part of the ileum become congested; during the second week 
these become pale and enlarged, due to proliferation of the lymph- 
oid cells and to phagocytic endothelial cells (macrophages) 
and softening and necrosis are apt to take place, which during 
the third week results in ulceration. When the Peyer's patches 
ulcerate, the ulcers are longitudinally disposed with reference 
to the long axis of the intestine (thus differing from the tubercu- 
lous ulcer in the same situation which is transverse). After the 
third or fourth week the ulcers begin to heal. Not all the lymph 
follicles or patches proceed to ulceration, and in some cases no 
ulcers are formed at all. In some cases the lymphoid structures 
of the upper colon and upper ileum are also involved. On the 
other hand the intestinal structures may not be involved, the in- 
fection electing lymphoid tissues elsewhere in the body as the 
seat of its activity. In typical typhoid fever, however, the in- 
testinal glands, the mesenteric glands, the spleen, liver, kidneys, 
bone marrow, and the lymphoid structures in other parts are in- 
volved, showing congestion, cellular infiltration, and frequently 
necrotic areas. The spleen is greatly enlarged (splenic tumor) 
in nearly all cases. 

The specific toxin is an endotoxin, to which the symptoms of 
temperature, delirium, prostration and anatomic changes are due. 
Agglutinins are also formed, and their presence after the first 
week of the disease may be shoAvn by the Wiclal reaction; viz., 
the clumping of the typhoid bacilli from a young culture when 
mixed with a minute quantity of the patient's blood serum. 



PATHOLOGY OF INFECTIOUS DISEASES 



175 



Antisera are of no avail therapeutically, but vaccination has 
proved successful as a preventive measure. 

After recovery, the organisms continue to grow in the liver 
and other parts of individuals, as well as in a few persons who 
never had the disease in recognizable form (subinfection). Such 
individuals may infect others, hence are called " typhoid car- 
riers." Diphtheria and a number of other infections may also 
be "carried" for variable periods of time. (Fig. 66.) 

Paratyphoid infection is a mild (rarely fatal) form which is 
clinically almost identical with typhoid fever, but with certain 
pathologic differences, and due to "paratyphoid" bacilli, of 




Fig. 66. — Typhoid fever, showing necrosis of Peyer's patches and intense congestion of 
the bowel. (Modified from East and Rumpel.) 



which there are several strains, and which differ from the B. 
typhosus in certain cultural characteristics and in agglutinative 
reactions. 

Bacillary Dysentery 

Bacillary dysentery is an infectious colitis due to B. dysen- 
teric (Shiga), a nonmotile member of the typhoid-colon group. 
It produces toxins which are probably both intracellular and ex- 
tracellular. Great swelling of the mucosa of the colon with muco- 
catarrhal inflammation are noted, and the surface of the colon 
becomes considerably eroded. In severe cases the inflammation 
becomes hemorrhagic and even necrotic, the alvine discharges 
varying in character with that of the inflammation. 



176 GENERAL PATHOLOGY 

Malta Fever or Mediterranean Fever 

Malta fever is a specific infectious disease, clinically resembling 
typhoid fever, and characterized pathologically by swelling of 
lymphoid structures, as Peyer's patches, spleen, etc., and with 
ulcerative inflammation of the large bowel, and due to the Micro- 
coccus melitensis. It is conveyed by means of the milk of infected 
goats, and probably in other ways. The disease is practically un- 
known in this country. 

Anthrax 

Anthrax is an infectious disease due to the B. antliracis, occur- 
ring in cattle and sheep (splenic fever) and communicated to man, 
in whom it is known as malignant pustule and wool sorters' dis- 
ease. 

Inoculation of the skin causes an intense local inflammation, 
consisting of a rapid infiltration of the part with leucocytes, great 
edema and large numbers of the bacilli. Pustules form which dis- 
charge a bloody fluid and become covered with crusts. The pus- 
tules or ulcers are intractable owing to rapid invasion of surround- 
ing tissues by the bacilli, which also enter the blood stream, and 
always cause a hemorrhagic splenitis. Any internal organ may be 
involved in the general infection. 

"When inhaled, as in wool sorters' disease, a severe, atypical lobu- 
lar pneumonia results, usually with involvement of the mediastinal 
tissues, endocarditis and pleurisy. 

A typical case of anthrax presents the most conspicuous example 
of septicemia or bacteremia (more specifically in this connection, 
a bacillemia) to be found in the study of infectious disease. Im- 
mense numbers of anthrax bacilli occur in the circulation, clogging 
the capillaries of organs and tissues, and apparently giving weight 
to the early theory that death was due to internal asphyxiation. 
Moreover no toxin, extracellular or intracellular, has been dem- 
onstrated. It is probable, however, that these bacilli, as all other 
pathogenic bacteria, form some kind of toxic substance, since death 
has occurred in some anthrax infections in the absence of large 
numbers of the bacilli in the blood vessels. Antisera have proved 
successful in some cases, while vaccination of cattle has been uni- 
formly successful as an immunizing measure. 



PATHOLOGY OF INFECTIOUS DISEASES 177 

Malignant Edema 

Malignant edema is an intense infection due to the B. e clematis 
maligni (Koch), characterized by rapid edematous swelling of the 
snbcntaneons tissnes with suppuration and frequently necrosis. 
The organism is anaerobic and does not enter the blood stream. 
Infection occurs through traumatisms, and is rare. 

Gaseous Edema 

Gaseous edema or infectious emphysema is an infection due to 
the B. aerogenes capsulatus (Welch). It causes an edema of the 
tissues with gas formation at the area of inoculation, usually the 
subcutaneous tissues. The whole body may be invaded. Rapid 
necrosis is apt to follow. Postmortem examination shows gas bub- 
bles in the internal organs and in the blood, rendering this fluid 
foamy. Infection takes place through abrasions of the skin or 
traumatisms, as compound fractures. The infection is very grave, 
but fortunately not very frequent. Postmortem gaseous edema 
takes place by invasion of the tissues from the intestinal tract, in 
which the bacillus is found as a parasite. 

Bubonic Plague 

Bubonic plague is a general infection due to the B. pcstis. The 
disease is common in the rat. ground-squirrel and other rodents, 
and transmitted to man by the rat flea and probably other insects. 
There are three forms of the disease: (a) the bubonic form, in 
which polyadenitis is the conspicuous feature. The bacilli are 
carried from the seat of inoculation to the nearest lymphatic glands 
which become swollen and inflamed (primary buboes). From these 
the bacilli are carried by the blood stream to the glands of the 
body generally (secondary buboes). There is a great tendency to 
capillary hemorrhage into the surrounding tissues, due to the 
action of the toxin upon the capillary Avails, setting up an intense 
hemorrhagic inflammation (periadenitis). The glands are greatly 
swollen, red and hemorrhagic; later they soften and suppurate. 
Microscopically the blood vessels are congested, inflamed and their 
lumen often plugged with bacilli. The lymphoid and endothelial 
cells are proliferated and the bacilli fill the lymph sinuses. 



178 GENERAL PATHOLOGY 

(b) The pneumonic form may result from the bubonic form or 
be directly contracted through inhalation of the virus from an- 
other diseased individual. A lobular form of pneumonia results, 
attended with marked edema and hemorrhages into the lung tissue. 
There is a mucopurulent bronchitis, and the peribronchial lymph 
glands are involved. This is the most fatal form of plague, as well 
as the most contagious. 

(c) The septicemic form is commonly the terminal condition of 
the bubonic and pneumonic forms, but at times plague septicemia 
occurs without distinct buboes or marked inflammation of the 
glandular tissues. 

In all forms the liver, kidneys, spleen and bone marrow are 
usually congested and enlarged, and show areas of hemorrhage, 
necrotic foci and the presence of the bacilli. 

The toxin is apparently intracellular. The use of antisera and 
of prophylactic vaccines has been more or less successful. 

Influenza 

Influenza is an infectious disease, often occurring in epidemics, 
less often in pandemics and characterized by inflammation of 
the respiratory tract, gastrointestinal tract, meninges and other 
parts. The exudate is mucopurulent, and often bloody. 

In 1892 Pfeiffer found in the blood and sputum of influenza 
patients a very small bacillus, which was named the B. influenzal 
and regarded as the specific cause of the disease. But the recent 
pandemic (1918-1919) has failed to confirm this view, the ma- 
jority of investigators apparently believing that the B. influenza? 
is merely an associated organism or secondary invader of the tis- 
sues. This bacillus is found in a majority of uncomplicated cases 
of influenza, and in the secondary pneumonia, endocarditis, otitis 
media, meningitis, etc., as well as in the blood. 

Pneumonia is the most frequent complication, and is usually an 
atypical and bilateral bronchopneumonia, of a more or less hemor- 
rhagic type. In some cases the areas involved are lobar rather 
than lobular in extent. The B. influenzal, pneumococci and strep- 
tococci, either alone or in association, are the chief causal factors 
of the pneumonia. 



PATHOLOGY OF INFECTIOUS DISEASES 179 

Epidemic Conjunctivitis 

Epidemic conjunctivitis ("pink eye") is a catarrhal or muco- 
purulent inflammation of the conjunctivae, due to the Koch- 
Weeks bacillus, which resembles the B. influenzae in morphology 
and staining reaction. 

Whooping Cough or Pertussis 

Whooping cough is a specific infectious inflammation of the 
upper air passages, occurring usually in childhood and character- 
ized by a paroxysmal, convulsive cough. A short oval bacillus 
was discovered in the bronchial exudate by Bordet and Gengou, 
and named B. pertussis. Later the organism was found in great 
numbers lying between the cilia of the tracheal and bronchial 
epithelium. It can be found in large numbers in the early stages 
of the disease, but later other organisms, especially the influenza 
bacillus, outgrow it. Bronchopneumonia is a frequent complica- 
tion of pertussis, and tuberculosis a moderately frequent sequela. 

Vincent's Angina 

Vincent's angina is an acute infectious inflammation of the 
tonsils, spreading to the pharynx, characterized by superficial 
ulceration and pseudomembrane formation, due to an anaerobic 
organism which in the early stage of its life history is a spindle- 
shaped bacillus (B. fusiformis) and later becomes a spiral form 
(Spirochccta vincenti) both forms appearing in the exudate and 
in artificial cultures. 

Relapsing Fever 

Relapsing fever is a specific infectious disease, due to the Spiro- 
ckceta obermeieri, and characterized by a peculiar febrile course; 
viz., three or four periods of five to seven days each of high tem- 
perature, separated by periods of equal length, in which the tem- 
perature is normal" or subnormal. 

The spirochete is usually classed among the flagellated protozoa, 
but Novy and Knapp have demonstrated that it has many of the 
characteristics of bacteria, and its classification must at present be 
considered as undetermined. 



180 GENERAL PATHOLOGY 

The spleen and lymphatic glands are enlarged and often the 
seat of various forms of degeneration or necrosis. The organisms 
occur abundantly in the blood, and were discovered by Obermeier 
in 1873. 

THE HIGHER BACTERIA 

(Trichomycetes, Chalamydobacteriaceae) 

These are filamentous forms (see page 153) which are inter- 
mediate between the true bacteria and the molds. Great confu- 
sion prevails in the classification and nomenclature of the organ- 
isms, but the following varieties are usually recognized: 
Leptothrix — thread-like filaments, showing no branching forms. 
Cladothrix — thread-like filaments, showing false branching forms. 
Nocarclia (Streptothrix) filaments, showing true branching forms. 
Actinomyces — radial filaments, showing true branching forms. 

The Nocardia form spores, which usually appear in chains; the 
actinomyces are further characterized by formation of club- 
shaped ends at the periphery of the rosette-like colony, and by 
the absence of spore-formation. 

The bacilli causing tuberculosis, diphtheria and glanders some- 
times exhibit branching forms, and are believed by many to be- 
long to the higher bacteria. 

Leptothrix Infections, (Leptotrichoses) 

The common saprophyte of the mouth (L. buccalis) may accord- 
ing to some observers become pathogenic and form white patches 
on the tonsils and other parts of the mouth. The organisms are 
regarded, however, by most pathologists as merely associated or- 
ganisms or secondary invaders. 

Cladothrix and Nocardia Infections or Mycoses 

The difference between true and false branching has not been 
definitely established; false branching being merely an apparent 
branching due to the fact that portions of fragmented filaments 
assume the position of branches to the main stem ; hence all that 
can be stated definitely at present is that organisms belonging to 
one or the other of these groups have been found in a causal 
relation in abscesses of the brain, in lesions of the lungs resem- 



PATHOLOGY OF INFECTIOUS DISEASES 



181 



bling tuberculosis very closely, and in other locations. Most ob- 
servers, however, are inclined to regard the pathogenic forms as 
belonging to the Nocardia (or Streptothrices), while the Clado- 
thrices are believed to be harmless saprophytes. 

Actinomycosis 

This is a chronic infectious disease due to the Actinomyces 
bovis. In cattle the lower jaw is principally affected ("lumpy 
jaw"), less frequently the upper jaw, tissues of the neck, the 
tongue ("wooden tongue") and rarely other parts. In man the 
disease occurs occasionally, affecting the mouth, lungs, and ab- 
dominal organs. 

The invasion of the organism results in the formation of a hard 
nodule which slowly increases in size and infiltrates and destrovs 




Fig. 67. — Actinomycosis of the tongue, a, actinomyces granule; b and c, cellular nodules; 
d, transverse section of muscle; a and /, connective tissue. (Ziegler.) 



adjacent tissues, whether these be soft tissues or bone. In the lungs 
the lesions often resemble tuberculosis. Microscopically there are 
round cell infiltration, proliferation of connective tissue cells and 
formation of granulation tissue rich in leucocytes. Occasionally 
giant cells appear. Later suppuration and necrosis result. Some- 
times repair processes proceed in one portion of the affected area 
while softening advances in another, causing considerable dis- 
figurement. 

Diagnostically the essential feature is the presence of the para- 
site itself, which is visible to the naked eye as a gray or yellow 
"sulphur granule." These granules crushed between two glass 
slides are seen to be composed of one or more rosettes made up of 



182 



GENERAL PATHOLOGY 



radially disposed filaments ("ray fungus") with club-shaped 
bodies at the periphery, and usually coccoid in the center, which 
may be degeneration products or contaminating cocci. (Fig. 67.) 

Mycetoma, or Madura Foot of India 

Mycetoma, or madura foot of India, is due to the Actinomyces 
madurae, which grows upon certain thorns whose prick causes 
the development of slowly growing, marble : like hard nodules on 
the foot, or rarely upon the hand. These nodules suppurate in 




Fig. 68. — Blastomycosis. Old partially healed ulcer of the leg. (Irons and Graham.) 

one or two years, the pus containing white, black ("melanoid 
form") or rarely red granules. 

Blastomycosis or Saccharomycosis 

Blastomycosis is an infection caused by yeasts (blast omycetes), 
a generic term for fungi which reproduce by budding. These cells 
are oval or spherical (1-40/*) and nucleated. Only a few yeasts 
appear to be pathogenic. The first fatal blastomycosis, reported 
in 1894, showed an ulcerous inflammation of the tibia, with metas- 
tasis to the internal organs and the lymph glands. A number of 



PATHOLOGY OF INFECTIOUS DISEASES 183 

cases of blastomycetic dermatitis have been observed; they begin 
as papules which ulcerate and spread, and run a chronic and 
usually fatal course. (Fig. 68.) 

Oidiomycosis 

Oidiomycosis is an extremely fatal disease, so far observed 
chiefly in the San Joaquin Valley, California. It was at first 
thought to be due to protozoa, and called coccidioidal granuloma, 
but is now known to be due to an organism resembling both yeasts 
and molds. Small tumor-like growths are formed, folloAved by 
fatal generalized infection in most instances. 

Thrush, or Soor, is a fungus growth found in the mouth, es- 
pecially of bottle-fed infants. White patches, composed of the 
organisms and epithelial debris, form on the palate and other 
parts. The causal organism — oidium albicans — grows on all media, 
forming both buds and mycelial threads, hence is regarded by 
some as a yeast, and as a mold by others. 

Mycoses due to Molds, or Hyphomycetes 

Hyphomycetes, or molds, are fungi characterized by growing 
in long threads or filaments (hyphce), which form a felt-like mass 
(mycelium). The hyphaB develop from single cells, often become 
branched, and finally at the tip of the terminal hyphre sporangia 
develop, which contain endospores. Some molds, however, form 
chains of budding exospores. 

Favus, or Tinea favosa is a dermatomycosis due to a mold — 
Achorion shoenleinii — which forms a yellowish moss-like growth 
on culture media. Favus is characterized by the formation of 
yellowish, concave, scaly crusts composed of the mold and des- 
quamated epithelium. The hair follicles in the diseased areas are 
usually penetrated by the mold. 

Ringworm, or Tinea trichophytina, is a mycotic inflammation 
of the skin, tending to spread in a centrifugal manner, and char- 
acterized by the formation of grayish, crusty rings of infiltrated 
inflammatory tissue, the center of which tends to heal while the 
peripheral part advances. The hair follicles are invaded by the 
organism, causing looseness and brittleness of the hairs. 

This dermatomycosis is due to the Trichophyton, of which there 
are two chief varieties, the microsporon with spores 2/* to 3'/* in 



184 



GENERAL PATHOLOGY 



diameter, found most frequently in ringworm of the scalp, and 
megalosporon with spores three times as large, found most fre- 
quently in ringworm of the body. The organisms are best ob- 
served by extracting a diseased hair in and about the root of 
which parallel rows of spores may be seen enclosed in delicate 
threads of hypha?. (Fig. 69.) 

Tinea tonsorans affects the scalp, and occurs most frequently in 
children. Tinea circinata affects the body, particularly the moist 
folds of the skin. Tinea sycosis, or "barber's itch" is a follicular 
inflammation of the hairs of the beard, attended with active in- 
flammation and often abscesses of the sebaceous glands. Tinea 







E 

-A 




s 






{If . ' M 




A — 


III a 






p'n 


— A 




*\ ;> :•• 






', Mi 






vi 






><%■:> 












, . ■ ♦ 4 \ m i 






;: ;* :\: 






f : ! -» 


.. 



Fig. 69. — Invasion of a human hair by trichophyton: A, Points at which the parasitic 
fungi coming from the epidermis are elevating the cuticle of the hair and entering into 
its substance. Magnified 200 diameters. (Sabouraud.) 



versicolor, or pityriasis, due to the fungus, microsporon furfur, 
consists of yellowish brown patches of desquamated epithelium 
in the upper layers of the skin, without active inflammation or in- 
volvement of the hair follicles. 

Sporotrichosis is a subacute mycotic inflammation of the skin, 
and sometimes of the mucous membrane, characterized by the 
formation of nodules resembling gummata (syphiloid type) or 
cutaneous tuberculosis (tuberculoid type) and often by multiple 
abscesses. When the mycosis becomes generalized, affecting 
deeper tissues or internal organs, it is apt to be fatal. The 
causal agent is a Sporothrix, which in lesions has the appearance 



PATHOLOGY OF INFECTIOUS DISEASES 185 

of oval yeast-like bodies, but in cultures forms long mycelial 
threads. 

Other molds, belonging to the genera, Aspergillus, Mucor, Peni- 
cillium, etc., have occasionally been observed in pathologic condi- 
tions, both local and general. The diagnosis of these mycoses, as 
in all cases of infection with the higher bacteria, yeasts and molds, 
rests upon the identification and demonstration of the organisms 
in the tissues. 

THE PROTOZOAN INFECTIONS 

Protozoa are unicellular animal organisms, ranging from 3 
micra to several centimeters in length. They contain one or 
more nuclei, and the cytoplasm presents an outer portion (ecto- 
plasm) concerned in prehension of food, excretion and locomo- 
tion, and a central portion (endoplasm), which is more granular 
and contains the digestive vacuoles and the nuclei. The major- 
ity of pathogenic protozoa have now been successfully cultivated. 

Protozoa are divided into the following classes: 

I. Rhizopoda (Sarcodina), which have changeable protoplasmic 
processes (pseudopodia). To this class belong the genera Ameba 
and Entameha. 

II. Mastigophera, which have flagella. The principal order is 
the Flagellata, to which belongs the genus Trypanosoma. 

III. Sporozoa, which have no flagella or cilia and which repro- 
duce by sporulation. Here are found the genera Plasmodium, 
Piroplasma and Coccidium. 

IV. Infusoria, which have cilia. The principal subdivision is 
the Ciliata, to which belongs the genus Balantidium. 

Amebic Dysentery 

Amebic dysentery is an infectious inflammation of the mucosa 
and submucosa of the large intestine, due to the Entameha his- 
tolytica, which measures 15 to 50/x and is round when at rest; its 
pseudopods are short and blunt, and its ectoplasm and endoplasm 
are well differentiated, thus differing from the Ameba coli (En- 
tameba coli), found in normal human intestines and regarded as 
harmless parasites; these are smaller and their ectoplasm and 
endoplasm are but slightly differentiated. 

The pathogenic amebaa are said to pass between the epithelial 
cells, enter the submucosa, causing inflammatory infiltration and 



186 



GENERAL PATHOLOGY 



fibrinous exudation, leading to ulceration. The whole colon or 
only localized areas may be affected. The ulcers vary in size from 
2 mm. to 2 cm., and have undermined edges, and yellowish red bases. 
The disease generally becomes chronic, and the submucosa greatly 
thickened. Stenosis of the colon may result from the healing and 
contraction of the ulcerous areas. 

The aniebas may enter the mesenteric blood vessels, reach the 
liver and cause focal necrosis or multiple abscesses, or occasionally 
a single large abscess. 

Amebse are frequently found in the mouth, in tartar of the 
teeth, in carious teeth, abscess of the jaw and in pyorrhea alveo- 
laris, but their causal relation to these conditions has not been 
proved. 



I 

> 


.. c 


Q 





Fig. 70. — Trypanosoma gambiense. (Todd.) 



Trypanosomiasis 

The trypanosomes include certain flagellates swimming free in 
the blood of man and animals. The cell body is elongated and 
averages 1.5 x 25/x. It has a long flagellum at the anterior end 
and an undulating membrane projecting from one side like a fan. 
Reproduction usually takes place by longitudinal fission. (Fig. 
70.) 

The following are the more common pathogenic trypanosomes: 

T. evansi, causing surra in horses and cattle — transmitted by flies. 

T. bruci, causing nagana in horses and cattle — transmitted by tsetse flies. 

T. cqui peril um, causing dcurine ("horse syphilis") — transmitted by coitus. 

T. gambiense, causing sleeping sickness of Central Africa — transmitted 
by the bite of the Glossina palpalis, a fly belonging' to the same genus as the 
tsetse fly, which causes nagana. 



PATHOLOGY OF INFECTIOUS DISEASES 187 

The T. gainbiense measures 1 to 2 x 17 to 25/x including the fla- 
gellum. The membrane usually crosses the body and motion is 
very active due to the screw-like rotation produced. 

Human trypanosomiasis occurs in two stages ; in the first the 
organisms occur in small numbers in the blood, but may be absent 
for days at a time. There is slight fever and glandular enlarge- 
ment. After several months or even several years, the second 
stage begins in which the patient becomes apathetic and drowsy, 
emaciation progresses and finally complete coma sets in, followed 
by death in six or eight months from the beginning of the second 
stage. The organisms are found in the blood and cerebrospinal 
fluid m this stage. The spinal fluid is cloudy, and the postmortem 
findings show a meningo-encephalomyelitis and enlargement of the 
spleen, liver and lymphatic glands. 

Leishmaniases 

The Leishmaniases include two tropical visceral and one cuta- 
neous disease. Kala-azar, or dumdum fever (India and Africa) is 
due to the Leishmania donovani, organisms belonging to the flagel- 
lates and related to the trypanosomes. The disease is characterized 
by splenomegaly, enlarged and cirrhotic liver, both organs being 
filled with the parasites, progressive anemia and remittent fever, 
running a course of six to nine months, with a mortality of 96 per 
cent. 

Infantile kala-azar or Splenomegaly is probably identical with 
the above type, occurring in the Mediterranean countries. 

Oriental sore or delhi boil is due to Leishmania tropica and 
characterized by ulcerating nodules on the face and elsewhere. 

Malaria 

Malaria is a protozoan disease, characterized by paroxysms of 
chills, fever and sweating, and anemia due to destruction of the 
red blood cells. It is due to the Plasmodium or Hematozoon ma- 
lariae (Laveran). 

This protozoon has two life cycles — one in man (the intermedi- 
ate host) and one in the Anopheles genus of mosquito (the true 
or definite host). When man is bitten by an infected mosquito, 
spores (or merozoites) of the Plasmodium enter his red blood 



188 GENERAL PATHOLOGY 

cells, grow upon its substance and dissolve its hemoglobin, until 
the parasite becomes as large or larger than the cell, swelling 
the latter until only a faint ring remains. Then division (seg- 
mentation or sporulation) takes place, occurring more or less 
simultaneously in all the organisms, thus accounting for the par- 
oxysms of the disease. Segmentation destroys the red cell, and 
the young protozoa escape into the blood plasma and each enters 
a new red cell to produce a second generation. While most of 
the organisms divide as just described there are some which 
grow to full size, destroy the red cell, but do not segmentate. 
These "extracellular bodies" are finally eliminated, unless a ma- 
larial patient be bitten by the mosquito and some of these bodies 
be sucked up with the blood. In the stomach of the mosquito, 
these bodies, which are sexually differentiated (gametocytes) 
find conditions favorable for sexual development; when the fe- 
male cell becomes fertilized, it penetrates the stomach wall and 
becomes encysted, and when the cyst ruptures the sporozoites 
migrate throughout the body of the mosquito, accumulating par- 
ticularly in the poison gland (a modified salivary gland) and 
are thus in position to be inoculated into man. 

Stagnant pools, swamps, etc., are not the habitat of the Plas- 
modium, but merely the breeding places of the mosquito. It is the 
female of about seven or eight species of the Anopheles genus by 
which infection occurs. 

The following features serve to distinguish the Anopheles from 
the common mosquito (Culex): 

The Anopheles The Culex 



The palpas of both sexes nearly The female palpa3 very short, 

equal to proboscis. the male palpse very long. 

In resting on perpendicular The body is parallel to the wall. 

wall, the body is inclined at 

angle. 

The wings are spotted usually. Wings never spotted. 

The head, thorax, and body Lower part of body is joined to 

form a straight line. thorax at an angle. 

The larva? are parallel to the The larva? hang downward from 

surface of the water. the surface of the water. 



PATHOLOGY OF INFECTIOUS DISEASES 189 

The Plasmodia are of three varieties : 

(1) P. vivax, causing* tertian fever, segmentates every 48 
hours, i. e., on the third day, into 12 to 24 merozoites. When 
young the organisms are hyaline and actively motile (ameboid), 
but as time for segmentation approaches they become granular 
and nonmotile. The fully grown parasite and the gametoeytes 
are larger than the average red blood cell. 

(2) P. malarial, causing quartan fever, segmentates in 72 hours, 
into 6 to 14 merozoites (usually eight.) The young parasites are 
not actively motile. The fully grown forms and the gametoeytes 
are about as large as the red blood cell. 

(3) P. falciparum, causing aestive-autumnal fever, a pernicious 
and often fatal type, occurs in two forms: (a) the quotidian which 
segmentates every day within the bone marrow and internal or- 
gans, into 6 to 16 merozoites. The young are actively motile. 
The fully grown forms and the gametoeytes (which are crescen- 
tic, "half -moon" forms) are smaller than the red cell, (b) The 
tertian form segmentates in 48 hours. This would cause the oc- 
currence of irregular paroxysms, but distinct paroxysms are sel- 
dom seen in this form of malaria. 

Gametoeytes with flagella may be seen in all types. 

The paroxysmal chills, fever and sweating are believed to be 
due to toxins liberated during segmentation. AYhen two groups 
of P. vivax segmentate on alternate days, daily paroxysms, or 
"quotidian fever," results. 

Pathologically, destruction of the red cells, with melanemia, 
relative and absolute leucopenia, and liberation and alteration 
of the hemoglobin are the principal features. Hemoglobinuria 
occurs, and the internal organs, as liver, spleen, bone-marrow and 
brain are darkly pigmented. The spleen is enlarged in all cases, 
soft and friable in acute cases, and filled with infected red 
blood cells; focal areas of necrosis are seen. In chronic cases 
the spleen may become enormous and sclerotic, with much of 
the pulp and follicles destroyed ("ague cake.") 

Texas cattle fever (''bovine malaria") characterized by acute 
fever and destruction of red blood cells, is due to the Piroplasma 
bigeminum, belonging to the Sporozoon class of parasites, which 
is transmitted by the cattle tick. 



190 GENERAL PATHOLOGY 

Coccidiosis 

Coccidiosis, primarily a disease of rabbits and occasionally 
transmitted to man, is due to the Coccidium oviforme, an ovoid 
granular body, enclosed in a tough capsule, and measuring 15 to 20 
by 20 to 40 micra. It occurs in the tissues, especially of the liver, 
where it forms cyst-like nodules, containing degenerated host cells 
in which the parasites are embedded. They are found also in the 
intestinal epithelium, and sporulate after elimination from the 
body in the stools. Infection may occur by ingestion of the spores. 
The liver besides containing the specific nodules becomes cirrhotic. 
Other organs are rarely involved. 

The Balantidium coli, an infusorial parasite, has been found in 
the intestines of swine and occasionally of man, and various patho- 
logic conditions, particularly colonic diarrhea, have been attrib- 
uted to it. It is found in the stools and blood, is ovoidal in form 
(0.06 to 0.1 mm.) and covered with numerous cilia. 

INFECTIOUS DISEASES CAUSED BY UNDETERMINED 
MICROORGANISMS 

Measles 

Measles (Rubeola) is an acute, contagious disease, due to a 
filterable virus, i.e., a microorganism small enough to pass 
through the pores of a porcelain filter, the filtrate causing the 
disease when susceptible animals are inoculated. 

Pathologically there is mild pharyngitis, rhinitis and conjunc- 
tivitis with a mottled eruption of the skin, consisting of brick- 
red, slightly elevated, papules, which run together to form cres- 
centic patches. The skin is hyperemic and slightly swollen, par- 
ticularly upon the face. The eruption is followed by a powdery 
desquamation. Both the eruptive lesions and the desquamated 
scales contain the virus, and may convey the disease, this being 
true also of other exanthemata, or diseases attended with char- 
acteristic skin eruptions. 

In severe cases of measles bronchopneumonia and nephritis may 
develop. In the severe and usually fatal form — the black mea- 
sles — the toxemia is great, and the eruption becomes hemorrhagic 
and dark. 



PATHOLOGY OF INFECTIOUS DISEASES 191 

German Measles 

German measles, or rubella, is a mild contagious disease, char- 
acterized by red punctate spots in the pharynx, followed by more 
or less circumscribed spots on tlie reddened skin, which do not 
fuse to form mottled patches, as in measles. Swelling of the 
postcervical glands is seen, and rarely there may be distinct 
pharyngitis, bronchitis, etc. 

Chicken Pox or Varicella 

Chicken pox, or varicella, is a mild contagious disease char- 
acterized by a red papular eruption which becomes vesicular. 
The papules are usually discrete and few in number, although 
occasionally they are numerous and may become very large, re- 
sembling pemphigus. 

Scarlet Fever or Scarlatina 

Scarlet fever, or scarlatina, is an acute contagious disease char- 
acterized by inflammation of the mucous membrane of the nose, 
mouth, throat and eyes, as in measles, but usually of greater in- 
tensity. The lingual papillae swell and redden ("strawberry 
tongue"), and the throat is spotted with fine red points. The 
rash, first appearing upon the body and spreading to the ex- 
tremities, consists of small red spols which fuse as the skin 
swells, thus forming an intensely red, uniform erythema. 

Endocarditis, pericarditis and nephritis, as well as broncho- 
pneumonia are more frequent than in measles, and the glands of 
the neck often suppurate. In fatal cases focal necrosis is usually 
seen in the internal organs. 

Mumps, or Acute Epidemic Parotitis 

Mumps, or acute epidemic parotitis is an acute contagious in- 
flammation of the parotid, less often of the submaxillar}' salivary 
glands. Usually the glands on both sides are affected, resulting 
in extensive and painful swelling, due to a serous exudation. The 
salivary ducts and the contiguous lymph glands are also usually 
inflamed, and metastatic orchitis and epididymitis are not in- 
frequent, especially in adults. 



192 GENERAL PATHOLOGY 

Measles, rubella, varicella, scarlatina and mumps are distinctly 
the diseases of childhood or youth. Their pronounced contagious 
character results in early infection, and the usual life-long immu- 
nity conferred makes second infections or recurrences and in- 
fections in adults very infrequent. 

Acute Poliomyelitis, or Infantile Paralysis 

Acute poliomyelitis, or infantile paralysis, is a disease of child- 
hood when occurring sporadically, but in epidemic form appar- 
ently affects any age, though still more frequent among the 
young. It is an acute general infection characterized by diffuse 
cerebrospinal lesions, especially inflammation of the anterior 
horns of the spinal gray matter, with paralysis and wasting of 
the muscles, degenerative changes in the nerves, hyperplasia of 
lymphoid structures and degenerative changes in the liver, lungs, 
kidneys, and other organs. 

The pia mater and arachnoid are inflamed, accompanied by 
marked round-cell infiltration; groups of ganglion cells become in- 
flamed, degenerate and disappear and their nerve fibers neces- 
sarily degenerate. The whole cord becomes edematous. In se- 
vere and fatal cases the medulla, pons, cerebellum or cerebrum 
are similarly affected. 

The virus is filterable and is present in the brain, cord, spinal 
fluid, nasopharynx, blood and gastrointestinal contents. Inocu- 
lated into the brain of a monkey, the symptoms and lesions of 
the disease are said to result. Small bacteria-like bodies have 
been discovered, but their nature and relation to this disease 
have not been fully established. Direct transmission through the 
nasopharynx to the nervous system is the most probable mode of 
infection according to Flexner, while Rosenau reported the trans- 
mission from monkey to monkey by the bite of the common 
stable fly. One attack of poliomyelitis confers immunity. 

Acute Articular Rheumatism 

Acute articular rheumatism is probably an infectious disease 
and apparently due to a streptococcus, but this has not yet been 
definitely established. The lesions consist of an arthritis, the in- 
flammation involving all the structures of the joint, and often 
the periarticular structures. The joints are usually involved in 



PATHOLOGY OF INFECTIOUS DISEASES 193 

succession (polyarthritis). The knee is the most frequently af- 
fected, then the ankles, elbows, and wrists. Endocarditis, peri- 
carditis or myocarditis are frequent complications. Sudamina 
are common, accompanying the profuse sweating, and subcuta- 
neous nodes (or aggregations of round or spindle cells) as large as 
buck shot may sometimes be felt on the fingers, wrists, elbows 
and elsewhere. 

Dengue 

Dengue is an acute contagious disease of tropical origin, which 
has invaded Europe, the United States, and South America. A 
mosquito is believed to be the contagium carrier, but fomites may 
also transmit the disease. There is a polymorphous eruption on 
the body, face, and arms, which may be scarlatiniform, urticarial, 
vesicular or even pustular. Many of the joints become swollen 
one after another and painful ("break-bone fever" and "dandy 
fever" — terms given in allusion to the peculiar gait necessarily 
assumed). The muscles become painful and swollen. Prostra- 
tion, convulsions and coma occur in fatal cases. One attack does 
not confer immunity, three or four recurrences being reported. 

Yellow Fever, or Typhus Icteroides 

Yellow fever, or typhus icteroides is an acute infectious dis- 
ease, endemic in American tropics and contracted through the 
bite of a mosquito — Stcgomyia calopus. The mosquito serves as 
a host for one of the life cycles of the microorganism, for an in- 
fected mosquito (one observed to draw blood from a yellow fever 
patient) can not infect a healthy person until after the lapse of at 
least 12 days. The unknown organism is in the peripheral blood 
only in the first three days of the disease, because a mosquito can 
convey the infection only when it bites the patient during that 
time; likewise only blood taken during that time will successfully 
inoculate a healthy person. The virus is filterable. One attack 
confers immunity. 

Pathologically there is fatty degeneration of the liver and acute 
hemorrhagic inflammation of the kidneys with degenerative changes 
in the parenchyma. Hemorrhages occur into the mucous and se- 
rous membranes: Icterus, albuminuria, hematemesis and fever 
with great prostration are the chief features. 



194 GENERAL PATHOLOGY 



Typhus Fever 



Typhus fever, or ship or famine fever is an acute contagious 
disease attended with a macular skin eruption (roseolas) later 
changing to copper-colored petechias, catarrhal inflammation of 
the air passages, intense toxemia with high temperature and severe 
nervous symptoms — the latter simulating those of typhoid fever. 
The spleen is enlarged, soft and easily ruptured. The liver is 
swollen, soft and grayish. In severe cases gastrointestinal 
hemorrhages, ulcerations of the esophagus and acute myocardi- 
tis are observed. In fatal cases the blood is dark and fluid and 
rapidly putrefies. The virus is believed to be transmitted by the 
body louse, Pediculus vestimenti, or "cootie." 

Smallpox, or Variola 

Smallpox, or variola, is an acute contagious disease marked by 
an eruption upon the skin of hard, shot-like papules, which 
change in a few days to vesicles, and finally to pustules. These 
pocks may remain discrete or become confluent. Finally the 
exudate of the pustule dries and a necrotic crust forms. When 
the lesions are confined to the epidermis no deformity or "pit- 
ting" results, but if the corium is much involved cicatricial 
scars are formed. Other changes that may occur are diffuse 
suppurative inflammation of the skin, ulcerations of the mucous 
membranes, ulceration of the lymph glands, degenerative changes 
of the liver, kidneys, and spleen. In the virulent form, Variola 
purpura, or "black smallpox," hemorrhage into the lesions or 
pocks occurs, giving them a purple or dark color, often inky black. 
In this form death may ensue before the pustular or even the vesic- 
ular stages are reached. 

Infection is direct by means of the eruptive lesions, especially 
the dried pustular exudates, but the blood, secretions and excre- 
tions may all convey the virus. One attack usually confers life- 
long immunity, and vaccination with the virus of cowpox gives 
immunity for variable periods ranging from one year to many 
years. 

Foot-and-mouth Disease 

Foot-and-mouth disease, or epidemic stomatitis, is a contagious 
disease of cattle communicable to man, occurring in Europe and 



PATHOLOGY OF INFECTIOUS DISEASES 195 

America. There is swelling of the mucous membrane of the 
mouth with formation of small clear vesicles, and similar lesions 
on the udders and hoofs. In man the mouth and hands are 
usually affected. The virus is filterable. One attack gives im- 
munity. Infection follows the use of milk or contact with af- 
fected animals. 

Rocky Mountain Fever 

Rocky mountain fever is an acute contagious disease observed 
in Montana, Idaho, Wyoming, and Nevada. It is characterized 
by epistaxis, fever lasting one to two weeks, bronchitis, nephri- 
tis, hepatic and splenic enlargement, slight jaundice, moderate 
leucocytosis, muscular pains and a macular rash over the body 
which does not disappear upon pressure (except at the begin- 
ning.) The virus is transmitted by a tick, Dermacentor reticula- 
ta or occidentalis, and is contained in the blood, but is not filter- 
able. 

METAZOA 

Among the Metazoa (multicellular animal organisms) the fol- 
lowing parasites are of interest to the pathologist. 
1. Helminthes, Vermes or Worms. — These are endoparasites, 

infestation with which is called Helminthiasis. They may be 

divided into : 

(A) Platyhelminthes, (Flatworms) — flat, bilaterally symmetrical, requiring 

two hosts for complete life cycle. 

Subdivided into: 

(a) Trcmatod.cs or Flukes — oval, leaf-like, unsegmented, having 

incomplete alimentary canal; majority hermaphroditic. 

(b) Cestodcs or Tapeworms — tape-like, segmented, no alimentary 

canal; all hermaphrodites. 
The Flukes include : 

(1) Distomum hepaticum, or Liver Fluke. 

(2) " buski, or Intestinal Fluke. 

(3) " pulmonale, or Lung Fluke. 

(4) Schistosomum hematobium or Blood Fluke. 
The Tapeworms include : 

(1) Tenia solium, or Pork Tapeworm. 

(2) " sagiiiata, or Beef Tapeworm. 

(3) Dibothriocephalus latus, Fish Tapeworm. 
(-t) Tenia echinococcus, or Dog Tapeworm. 

(5) " nana, or Dwarf Tapeworm. 

(6) " canina, or Dog and Cat Tapeworm. 



196 GENERAL PATHOLOGY 

(B) Nematodes or Bound Worms — elongated, cylindrical, tapering toward 
ends, bisexual in nearly all cases, the female being twice as large as 
the male. These include: 

(1) Ascaris lumbrieoides — Common round worm. 

(2) Oxyuris vernricularis — Thread or seat-worm. 

(3) Trichocephalus dispar — Whipworm. 

(4) Strongyloides Intestinalis (Anguillula). 

(5) Ankylostoma duodenale or Hookworm. 

Uncinaria americana — American Hookworm. 

(6) Trichina spiralis. 

(7) Filaria medinensis — Guinea-worm. 

(8) ll sanguinis hominis (F. bancrofti). 

(9) Eustrongylus gigas. 

II. Arthropoda (having "jointed feet"). These are epipara- 
sites, which cause various forms of dermatitis. Some are dis- 
ease carriers. 

(A) Arachnida — "spider-like" forms, air-breathing: 

(a) Acari — including mites and ticks. 

(i ) Mites (1) Leptus autumnalis — Harvest mite. 

(2) Acarus scabiei — Itch mite, 
(ii) Tides (1) Dermacenter reticularis — believed to be car- 
rier in Rocky Mountain Fever. 
(2) Margaropus aimulatus — believed to be car- 
rier in Texas cattle fever. 

(B) Insecta — having "cut into" or segmented bodies. 

(1) Pediculus capitis or Head louse. 

(2) lt pubis or Crab louse. 

(3) " vestiinenti or Body louse, "cootie." 

(4) Cimcx lectularius or Bed bug. 

(5) Pulcx irritans or common Flea. 

(G) " penetrans or Jigger, Cliigger, or Chigoe. 

(7) " cheopis or Eat ilea of India, Australia and the Phil- 

lipines, believed to convey B. pestis which causes bubonic 

plague. 

Trematodes. — The ova are deposited in water and developed 
into ciliated embryos (miracidia), which enter a small snail (mol- 
lusk) in which they develop into motile bodies (cercariae). These 
leave the mollusk (intermediate host), and swim about in the 
water, whence they may enter man (definitive host). 

Of the many fluke-worms the following only are important: 
Distomum hepaticum, or Liver fluke, is oval (8x25 mm.) hav- 
ing two suckers ("distomum") and a median genital pore con- 
taining male and female organs (hermaphrodite). The mature 
fiuke-Avorm, yellowish brown or pink in color, is found in the 



PATHOLOGY OF INFECTIOUS DISEASES 



197 



bile ducts of herbivora, rarely in man, and if in sufficient num- 
bers, will cause obstructive inflammation of the ducts. In sheep 
the liver is often greatly degenerated ("liver rot.") (Fig. 71.) 

Distomum buski is the largest fluke-worm found in the human 
intestine (25-70x5-14 mm.); occurs chiefly in Eastern and South- 
ern Asia. 

Distomum pulmonale (Paragonimus westermani) or Lung 
Fluke. — This is about one-third as large as D. hepatica, and 




Fig. 71. — The common liver-fluke (Fasciola hepatica), enlarged to show the anatomic 
characters. (After Stiles.) 



found in cyst-like cavities in the lungs. It is apt to cause hemop- 
tysis (parasitic hemoptysis of Eastern Asia). 

Schistosomum hematobium, or Blood Fluke. — This worm is bi- 
sexual, the male measures 12x0.5 mm., and is white in color, the 
female, 20x0.25 mm., is white anteriorly and gray posteriorly. 
The female is attached to the male, lvine in a groove on the ven- 



198 



GENERAL PATHOLOGY 



tral surface of the latter. They occur in the veins of the bladder 
and rectum (very rarely entering the general circulation), and 
cause local inflammation, ulceration and hematuria (Bilhar- 
ziasis of Africa and Asia). The ova, yellow, translucent and oval 
(1 mm.), may often be found in the urine or feces. 

The Cestodes, or Tapeworms 

Tenia Solium, or Pork Tapeworm. — This parasite is 2 to 4 me- 
ters long, occasionally much longer, and consists of a small head 
(1 mm.), spherical and dark brown in color, (scolex), with four 
disc-like suckers and a rostellum armed with a double row of 
hooklets (about 30) on its anterior end. The neck is thread- 
like and one inch long. The body (strobila) is composed of 600 




Fig. 72. — Head of Taenia solium. (Mosler and Peiper.) 

to 900 segments (proglottides) which increase in size from the 
neck backward, becoming smaller again near the posterior end. 
The largest segments measure about 6x10 mm. Each segment 
(proglottis) is hermaphroditic and has a uterus with seven to fif- 
teen branches. Groups of segments may be discharged from the 
boAvel at intervals, and each segment has independent motility. 
The ova develop in utero into embryos having six hooklets, and 
surrounded with a striated shell (onchosphere). "When ingested by 
the hog, or rarely other animals, even man, the shells are dissolved 
in the stomach and the embryos pass into the tissues where they 
form cysts (cysticerci) and develop a scolex. The cysts are visible 
to the naked eye, and constitute the "measled" pork or other 
meat. "When insufficiently cooked pork is eaten, the scolex or head 



PATHOLOGY OF INFECTIOUS DISEASES 199 

attaches itself to the mucosa of the upper ileum and a tapeworm 
develops, reaching its full growth in about four months. (Fig. 
72.) 

Tenia Saginata or Beef Tapeworm. — This is twice as long and 
has a head twice as large as the T. solium. The head has four 
suckers, but no rostellum or hooklets. The segments usually 
number over 1000, the largest measuring 7x20 mm. The uterus 
has 20 to 35 branches, and the ova are larger and more oval than 
those of T. solium ; the segments also are more motile. The lar- 
vge are found in the muscles, liver, and lungs of the ox. 

Dibothriocephalus Latus or Fish Tapeworm. — This is the larg- 
est parasite of man. It is common in Asia and Europe, is gray- 
ish yellow in color, measures 5 to 9 meters in length and has 
3000 to 4000 segments, short and broad in the middle but di- 
minishing toward either end. The head is very small, flattened, 
elongated and has a deep, longitudinal groove on each side. The 
ova have brown, operculated shells, and develop in the water to 
motile, ciliated embryos, provided with six hooklets, which enter 
an intermediate host, usually the pike, perch or other fresh- 
water fish. The complete life history of this worm is not known. 

The S} T mptoms produced by the larger intestinal tapeworms 
are usually insignificant, and in the majority of instances these 
worms occasion no harm; however, when present in great num- 
bers, they may cause intestinal obstruction, and various reflex 
nervous symptoms, and occasionally grave anemic conditions, 
believed to be due to hemolytic poisons formed by the death and 
decomposition of portions of the worm. 

Tenia Echinococcus. — This is a small tapeworm, 2 to 6 mm. 
long, inhabiting the intestines of dogs, wolves, foxes, etc. It is 
composed of a head and three segments. The head is about one- 
third as large as that of T. solium, but otherwise resembles it in 
structure and equipment. The last segment alone is mature, and 
as large or larger than the remainder of the worm. The uterus 
consists of a central trunk with lateral branches. The ova are 
thin-shelled and resemble the ova of the pork tapeworm. When 
ingested by man the embryo passes to the liver, lungs and other 
parts, forming a cyst — the hydatid cyst. 

The hydatid or echinococcus cyst has a wall composed of two 
layers, an outer layer of elastic cuticle (ectocyst) and an inner, 



200 GENERAL PATHOLOGY 

germinal layer, (endocyst). The entire cyst becomes encapsulated 
by fibrous tissue from the tissues of the host. From the inner 
germinal layer, bud-like "brood capsules" develop and project 
into the cavity of the cyst ; from the brood capsules scolices (heads 
with suckers and hooklets) form as external growths. The inte- 
rior of the cyst is filled with clear fluid, nonalbuminous, but rich in 
sodium chloride and other salts. 

From the primal or "mother cysts," secondary cysts, "daugh- 
ter" and even "granddaughter cysts" may develop, each capable 
of forming brood capsules and solices. Thus from one ovum, 
thousands of solices may develop. Hydatid cysts vary in size from 
a walnut to an apple ; occasionally they grow to a very large size, 
especially when secondary cysts arise. "When large they are apt 




Fig. 73. — Taenia echinococcus, enlarged (Mosler and Peiper). 

to rupture into the peritoneum, lungs and other organs or struc- 
tures with fatal results. Small cysts may become inactive after 
a time, or die and be replaced with fatty, fibrous or calcareous ma- 
terial. (Fig. 73.) 

Tenia nana, or dwarf tapeworm, is one inch long, often less, 
occurring in rats and other animals and rarely in man. The inter- 
mediate host is believed to be an insect. 

Tenia canina is a worm found in dogs and cats, sometimes in 
man, especially children. It is 15 to 35 cm. long; its head has 
four suckers. The mature segments are reddish in color, and re- 
semble cucumbers in shape, hence also called T. cucumerina. 

The Ascaris lumbricoides is a frequent parasite of man, par- 
ticularly of children. The female ascaris measures 20 - 35 cm. 
x 4~6 mm. These worms are brown or pink in color, cylindrical 



PATHOLOGY OF INFECTIOUS DISEASES 



201 



and nonseginented, resembling the common earth worm in out- 
line. They are transversely striated and have four longitudinal 
ridges. The head is small, and the mouth is surrounded with 
three lips. The tail of the female is straight, that of the male 
is curved. Infestation occurs through ingestion of the ova, which 
develop into worms in the upper and middle portions of the ileum. 
Usually only a few worms are present at one time, and these 




Fig. 



'4. — Ascaris lumbricoides: A, female; B, male; C, egg, magnified 300 diameters; 
b, head, magnified. (After Perls.) 



may cause few or no symptoms, but sometimes great numbers 
occur and may cause obstructive symptoms, or may migrate into 
the gall ducts, stomach, esophagus, trachea and nose. Fatal 
plugging of the pharynx has occurred. The parasite secretes 
irritating, volatile aldehydes and fatty acids, which may account 
for the anorexia and nervous manifestations that frequently oc- 
cur. (Fig. 74.) 



202 GENERAL PATHOLOGY 

Oxyuris vermicularis, or Pin-worm, Thread-worm or Seat- 
worm. — These worms are small, white, round, the female meas- 
uring 10 x 0.4 mm. and having a straight posterior end, that of the 
male being curved. These parasites are very common in children. 
Infestation occurs through ingestion of the ova, and the worms 
mature in the small intestine. After impregnation the female 
descends into the rectum where the eggs are deposited. 

Many of the ova and worms are discharged with the feces, 
but some of the latter pass out per anum by their own movements, 
causing considerable irritation and nervous irritability. Emi- 
gration occurs principally at night and the parasites are often 
found upon the bed clothing. 

Trichocephalus dispar or Whipworm. — The anterior end of this 




Fig. 75. — Male Trichocephalus dispar or whipworm. A large part of the cephalic end 
has transfixed a fold of intestinal mucosa. (Cohen.) 

worm is thread-like, resembling the lash of a whip, and the pos- 
terior part is thicker ("handle") and straight in the female, but 
curled in the male. The female is 45 to 50 mm. long, the male 
a few millimeters less. The ova incubate in water or mud. 
When ingested the embryo develops and matures in the cecum, 
occasionally entering the appendix. The worm attaches itself by 
penetrating or transfixing a fold of mucous membrane with its 
thin anterior end. It is a frequently encountered parasite, and 
usually quite harmless, but occasionally serious anemia has been ob- 
served. (Fig. 75.) 

Strongyloides intestinalis ( Aguillula intestinales) .—These 
small (2x0.30 mm.) worms occur in the upper intestinal tract in 



PATHOLOGY OF INFECTIOUS DISEASES 



203 



association with certain forms of diarrhea in the tropics, but 
its etiologic significance is not definitely determined. 

Ankylostomiasis, or Uncinariasis, is a disease due to the pres- 
ence of the hookworm. It is characterized by anemia, which in 
some cases resembles the pernicious type ; the cells are greatly 
reduced in number and many nucleated red blood cells appear. 





Fig. 76. — Cephalic extremity of Uncinaria Duodenalis. Profile and front view. (After 

Eeuckart-Gould.) 




Fig. 77.- 



-Duodenum showing attached Uncinaria. (Specimen of Capt. C. F. Kieffer, U. S. 
A., presented to the Jefferson Medical College.) 



The bone marrow is pale and fatty or gelatinous. The leucocytes 
are not increased, in fact may be decreased but the eosinophils 
usually rise to 15 or 25 per cent of the total leucocytes. 

The hookworm attaches itself to the duodenum or upper 
jejunum, causing the loss of blood by hemorrhage and by ab- 
sorption, and produces hemolysins. The patient becomes sal- 



204 GENERAL PATHOLOGY 

low, debilitated and usually exhibits epigastric pain and tender- 
ness, with dyspnea and other symptoms. Children become stunted 
in growth. The disease prevails in tropical and subtropical 
countries — India, Egypt, Southern Europe, West Indies and the 
southern part of the United States. 

The hookworm or Ankylostoma duodenale is a short, white 
worm — brown or red when gorged with blood — its head bent back 
like a hook, and its mouth having six hook-like teeth. The female 
is 10 to 18 x 1 mm., the male being about one-third smaller, and 
having at its posterior end an expanded copulatory bursa. The 
ova when discharged incubate in moist, warm soil and the re- 
sulting larvae penetrate the skin of the feet of those who work 
in or pass through the contaminated soil. The parasite then 
reaches the lungs and passes by way of the trachea and the 
esophagus into the intestines. (Figs. 76 and 77.) 

The Necator Amcricanus, or American, or New World, Hook- 
worm, is a separate genus, found in the southern part of the 
United States, South America and other parts. It is smaller in 
size and has plates or suckers in place of the hook-like teeth 
of the Old World hookworm, and its ova are larger, but it has 
practically the same life history and produces the same symp- 
toms and pathologic changes. 

Trichinosis (Trichiniasis) is a parasitic disease attended with 
painful myositis and extensive edema, due to the presence of the 
larvae of the Trichina spiralis. The larvae are ingested by those 
who eat insufficiently cooked, trichinosed pork. The larvae lie 
curled and encysted in the muscles, where they can remain alive 
for many years, and when ingested by man or other animals 
the capsules are digested and the embryonal worms liberated. 
They mature in the small intestine where the females (3 to 4 
mm. long and twice the size of the males) are fecundated, after 
which the males die. Within a week 1000 to 2000 embryos are 
born, which enter the lymph and the blood streams, finally lo- 
cating in the muscles and become encysted, in which stage they 
are identical with the encysted stage in the hog. Hogs probably 
become infected by eating offal. 

In two or three days after eating diseased meat, nausea, vomit- 
ing, pain, and diarrhea usually occur. In the invasive stage there 
is fever, and in severe cases symptoms resembling typhoid fever 



PATHOLOGY OF INFECTIOUS DISEASES 



205 



are present. Acute myositis with mild or severe pain and in- 
terference with muscular function are always noted, and leuco- 
cytosis with eosinophilia constituting 30 to 50 per cent of the 
total white cells is almost a pathognomonic sign. The mortality 
is 5 per cent, but in certain epidemics it is much higher. (Fig. 
78.) 

Guinea-worm Disease (Dracontiasis) is a tropical disease due 
to the guinea-worm (dracuncuhis medinensis) . Man is infected 
by the Cyclops (a minute fresh-water crustacean) and the em- 
bryos develop in the intestinal tract; after fecundation the male 
dies and the female enters the tissues through which it slowly 
migrates, finally (8 to 16 months) reaching the region of the an- 
kles, where vesicles or ulcers form, through which the worm dis- 
charges her embryos periodically, after which it passes from the 




frnn|jjfl 



Fig. 78. — Trichina spiralis with 



its connective-tissue covering 
fied. (Leuckart.) 



early stage; b, calci- 



body through the same lesions and dies. The embryos enter 
the cyclops as their intermediate host, 

Filariasis is a disease caused by various filaria, Avhose larvae 
are found in the blood, while the parent worms are found in 
the tissues, the inner blood and lymphatic vessels and lymph 
glands. 

The Filaria oancrofti (F. sanguinis hominis nocturna) is a white, 
uniformly cylindrical worm, the female having a curved tail and 
the male a spiral tail. The female gives birth to larvae (0.3 mm. 
x 8/x) which pass into the lymph stream, thence into the blood 
and may be seen in samples secured at night (or in daytime if 
the patient sleeps during the day) as small, snake-like worms 
whose active movements agitate the red corpuscles. In the day- 
time they recede into the lungs and larger blood vessels. These 
larvae (microfilaria) may remain in man for years, being unable 
to become mature worms until they enter a suitable intermediate 



206 GENERAL PATHOLOGY 

host — the Culex genus of mosquito, which may occur when a pa- 
tient is bitten during a time when the larvae are in the peripheral 
blood. In the mosquito the larvae undergo several developmental 
changes and finally pass into the proboscis whence they may be 
inoculated into man. 

Pathologically the filaria may occasion no symptoms, though 
eosinophilia is always present, but in other cases the parent 
worms, which lie curled up in the larger lymphatic vessels, trunks 
or even the thoracic duct cause obstruction of the vessels, lead- 
ing to distention of tributary vessels; secondary inflammatory 
thickening may occur, with distention and rupture of the lym- 
phatics of the kidneys, bladder or other structures, causing 
hematochyluria, or of the scrotum, causing chylocele, etc. When 
very extensive the obstruction may extend to the peripheral lym- 







Fig. 79. — Filaria embryo, alive in the blood. (F. P. Henry.) 

phatics with great distention of the tissues, known as Elephan- 
tiasis, which usually affects the lower limbs, scrotum, and less 
often other parts. (Fig. 79.) 

The Eustrongylus gigas is a brownish or red worm (the female 
may be 100 cm. long) which is found in the pelvis of the kidney, 
ureters and bladder of cattle and rarely of man, causing dilata- 
tion of these structures with atrophy of their substance. 

Leptus Autumnalis is a name applied to the larvae of the harvest 
mite and other mites ; they possess a suctorial proboscis with 
which they penetrate the skin and cause greater or less irrita- 
tion. 

Acanis sedbiei, or Itch-mite, is a pale, spheroidal body with 
bristly legs. The male (0.2 to 0.3 mm.) lives upon the surface 
of the skin, but the female (0.3 to 0.4 mm.) after impregnation 
burrows into the epiderm (thus becoming an endoparasite tern- 



PATHOLOGY OF INFECTIOUS DISEASES 



207 



porarily) laving her eggs at intervals in the epidermal tunnel, 
which appears as a dark line about one centimeter long, and 
oftenest located between the fingers, on the wrists, elbows, axillae, 
etc. Vesicles and sometimes pnstnles form along the course of 
the bnrroAv. The ova hatch in a few days, forming six-legged 
larvae. (Fig. 80.) 

The pathologic manifestations produced by the Insecta may be 
summarized in the statement that some of them cause more or 




Fig. 80. — Female acarus (after Anderson). 



less annoyance by injecting an irritating salivary secretion when 
they bite, which occasionally causes eczema, but more often 
leads to secondary bacterial infection due to the scratching in- 
duced by the itching. 

The female jigger (Pnlex penetrans) after impregnation bur- 
rows beneath the skin, as does the Acarus scabiei, especially be- 
tween the toes, where she lays her eggs, causing inflammation 
and often ulceration. 



CHAPTER IX 1 

MALFORMATIONS 

The term ''malformation'' is used to designate an abnormal de- 
viation from the usual structure of parts or organs and is the 
result of errors or accidents in the process of development. 

The study of malformations, therefore, is primarily the study 
of embryology, because they occur during the process of intra- 
uterine development. 

While we have as yet no classification that is entirely satis- 
factory, the following is perhaps the best for the student. 

1. Malformations by Excess. — The excess may be simply a re- 
dundant foreskin or a supernumerary digit, or it may be an al- 
most completely formed individual (double monster). Gigantism 
also comes under this head. 

2. Malformations by Defect include those due to arrest of the 
normal process of development, and they fall into three groups: 

(a) Those due to defective development in the posterior median 
line. 

(b) Those due to defective development in the anterior me- 
dian line, including the structures of the umbilical cord. 

(c) Miscellaneous defects involving chiefly the internal or- 
gans. 

3. Malformations by Perversion include those cases in which 
the development has been irregular or disorderly. 

Malformations by Excess 

In Double Monsters the duplication may be anything from an 
arm or leg to the entire body. In the latter event, if the de- 
velopment of the individuals is equal, two well-formed children 
result (homologous twins) ; but if one is stronger than the other, 
it develops at the expense of the weaker, which shrivels up or 



1 This chapter lias been written by J. Walter Reeves, M.D., formerly Professor 
of General Pathology in the Dental Department of the University of Southern 
California. 

208 



MALFORMATIONS 209 

only partially develops. When there are two individuals, they 
are usually united by corresponding parts, and the monster is 
named according to the location of the union; for example, when 
it is at the head, craniopagus; at the sternum, sternopagus; at the 
xiphoid, xiphopagus (Siamese twins); etc. 

Malformations by Defect 

(a) Malformations Due to Defective Development in the Pos- 
terior Median Line. — 

1. Those due to failure of the neural groove to form the neural 
canal. 

(a) Anencephalocele, in which all the brain is missing. 

(b) Open spina bifida, an absence of all the structures covering 
the medullary canal. 

These two forms are incompatible with life, and of little in- 
terest. 

(c) A minor degree of spina bifida. These cases show a tumor 
in the lumbar region, which may contain: (1) a cavity continuous 
with the central canal and surrounded b} T all the structures of the 
cord (syringomyelocele) ; (2) part of the cord with its membranes 
(myelomeningocele) ; or (3) only the cord membranes {menin- 
gocele). 

(d) Similar pouches in connection with defects in the cranium, 
which may contain (1) a cavity continuous with one of the ven- 
tricles and surrounded by brain tissue and the membranes (cn- 
cephalocele) ; (2) brain tissue and membranes (cnccphalomcnin- 
gocele) ; or (3) membranes only (meningocele). 

2. Malformations occurring after tiic cranium and spinal canal 
are formed. 

(a) Microencephalia. (small brain) and micromyelia. 

(b) Irregular defects of the cortex. 

(c) Hydrocephalus, in which there is an abnormal increase in 
the amount of fluid in the ventricles (internal hydrocephalus) or 
surrounding the brain (external hydrocephalus). The cranium 
may reach an enormous size. 

(b) Malformations Due to Defective Development in the An- 
terior Median Line. — 

1. Irregularities in the fusion of the maxillary and nasal proc- 
esses. 



210 



GENERAL PATHOLOGY 



Harelip and cleft palate, which will he taken up in detail later. 

2. Irregularities in the closing of the branchial clefts. Fistida 
in the neck. 

3. Umbilical hernia. 

4. Meckel's diverticulum is formed by the persistence of the 
omphalomesenteric duct, and is given off from the ileum between 





Fig. 81. 



Fig. 82. 



Fig. 81. — Head of fetus at end of fifth week. (After His.) C, frontonasal process; B, 
maxillary process; A, mandibular processes. 

Fig. 82. — Head of fetus in the seventh week. (After His.) A, the now united man- 
dibular processes; B, the maxillary process; C, frontonasal process; D, lateral nasal proc- 
ess; E, globular processes attached to the nasal part of the frontonasal process. The 
central nasal processes are separated from the lateral on each side by the lateral nasal 
grooves, which represent the anterior nares. 

12 and 36 inches from its lower end. It is present in about 2 per 
cent of persons. 

5. Vesical fistula, the bladder opening through the anterior ab- 
dominal wall. 

6. Epispadias, the urethra opening above the penis. 

7. Hypospadias, in which the urethral opening is on the under 
surface of the penis or through the scrotum. 

8. Imperforate anus. 



MALFORMATIONS 



211 



(c) Miscellaneous Defects. — One or both kidneys may be lob- 
ulatecl or horseshoe-shaped, the testicles undescended, viscera 
transposed, etc. 

The various forms of clubfoot, intrauterine amputations and 
congenital hip dislocation may also be classed under this head. 

Malformations of Perversion are too numerous and varied to 
be described in detail. 




84. — Almost complete single harelip. 




Fig. 85. — Diagram of median hare- 
lip. (After P.lair.) 

Harelip and Cleft Palate 

These malformations are due to a failure of complete union 
of the maxillary and nasal processes. (Figs. 81 and 82.) 

Harelip involves the upper lip, and is usually, though not al- 
ways, complete, through the entire lip into the nostril. It may 
be single or double, and is very rarely in the median line. It 
may or may not be associated with cleft palate. Figs. 83'. 84, 
and 85.) 

Cleft palate may involve the soft palate only, or both hard 
and soft palates, and may be either single or double. The va- 
rious forms are shown m Fia's. 86 and 87. 



212 



GENERAL PATHOLOGY 




Fig. 86. — Cleft of the hard and soft palate. (Federspiel.) 




Fig. 87. — Complete double cleft in an infant. (Blair.) 



PART II 
DENTAL PATHOLOGY 



CHAPTER X 
INTRODUCTION 



Dental pathology is the study of dental and oral disease in all 
of its aspects. Dental and oral disease is any structural or phys- 
iologic deviation from the normal in the hard tissues of the teeth, 
in the pulp, in the peridental membrane, in the supporting os- 
seous structures (i.e., the alveolar process), in the gingivae and 
gums, in the soft tissue lining of the mouth, and in the salivary 
glands. 

The study of the anatomic changes in cells, as the results of 
disease-producing influences, is concerned with morbid anatomy 
and morbid histology, or as generally termed, pathologic anatomy. 
The study of altered function resulting from abnormal degrees 
of irritation of any kind is concerned with morbid or pathologic 
physiology. We shall endeavor throughout the book to discuss 
dental diseases from both viewpoints. 

The conditions giving rise to disease, whether predisposing or 
exciting, are included in the study of etiology, which has refer- 
ence to the cause, or group of causes which give rise to ana- 
tomic or physiologic deviations from the normal. 

Predisposing and Exciting Causes 

If man were to live a better regulated life than is generally 
possible in this age of intense physical and mental needs, par- 
ticularly so in regard to proper diet, clothing, ventilation, ex- 
ercise, rest, both physical and mental, and sleep — doubtless the 
toll of disease would be much less than is actually the case. The 
functions of the tissues and organs of the body would be car- 

213 



214 DENTAL PATHOLOGY 

ried on, after the stage of maturity had been reached, in such 
a way as to make up for functional disuse without undue stress 
on any of the body structures, and this state of functional balance 
would be accompanied by the expression of a maximum of power 
on the part of the cells and fluids of the body to resist bacterial 
infection. The vital resistance would be at its highest. As it is, 
the degree of vital resistance varies frequently, at times being 
high (i.e., non-receptivity to bacterial infections), and at others 
below par, or low (i.e., receptivity to bacterial infection). A de- 
gree of vital resistance below the maximum for a given individual 
predisposes to and makes possible the onset of disease. 

Lowered Vital Resistance 

The conditions which lower vital resistance are improper cloth- 
ing, extremes of temperature, errors of diet in either quantity 
or quality of food, faulty metabolism (defective assimilation, 
elimination or both), excessive use of alcoholic beverages, poor 
ventilation of living quarters, continued dampness, mechanical 
and thermal irritation, foci of chronic infection, chemical poisons, 
addiction to drug forming habits, anatomic abnormalities, men- 
tal depression, etc. In the presence of any one or more of the 
foregoing conditions the power of the human organism to ward 
off a bacterial invasion is minimized, and the microorganisms 
which first enter any portion of the body, being enabled to prop- 
agate the infection soon acquires a degree of virulence which 
is manifested in various kinds and degrees of cell degeneration 
or death. Vital resistance below par renders the individual sus- 
ceptible to disease. 

Exciting Causes 

AYhile some of the conditions enumerated under the heading of 
predisposing causes play an important role in the development 
of disease of bacterial origin, it is to be borne in mind, however, 
that there are diseases whose etiology can not be directly as- 
sociated with the presence of bacteria. It is then that abnormal 
food supply, sudden extremes in temperature, mechanical forces, 
chemical poisons, congenital anatomic deviations, and changes 
in the external or internal secretions — all of these without bac- 
terial infection, have to be included in the group of exciting 



INTRODUCTION 215 

causes. That is to say. any one or more of the nonbacterial 
factors may incite a diseased state regardless of any bacterial 
activity. In the so-called diseases of metabolism, for instance, 
pathogenic bacteria are, strictly speaking, not concerned, and 
if concerned, are secondary to the primary etiologic causes. The 
condition of the individual will depend upon the normal or ab- 
normal assimilation of food, this being governed by the quality 
and quantity of the digestive secretions. Again, pathogenic 
bacteria are excluded as causative factors in such pathologic con- 
ditions as rickets, myxedema, cretinism, exophthalmic goiter, 
Addison's disease, hyperglycemia, diabetes, arteriosclerosis, val- 
vular disorders, etc. 

Predisposing Causes of Dental Disease 

In diseases of the teeth and associated structures, the predispos- 
ing cause may be found in an impairment of circulator)/ activity. 
This is often brought about by the existence of a systemic dis- 
order. Consequently, that which from the standpoint of the phy- 
sician is the manifestation of an exciting cause — disease — from 
that of the dentist it must be considered as the predisposing cause 
of the dental and oral disorder. "We know. I'm- instance, that 
after the removal of all sources of irritation to the peridental 
membrane, alveolar process, and gingivae in a case of true pyor- 
rhea alveolaris, not infrequently the pathologic process con- 
tinues. The structures concerned at no time develop the max- 
imum of vital resistance necessary to overcome the bacterial ele- 
ment concerned in the process. This lessened resistance in the 
supporting tissues may be the result of abnormal circulation fol- 
lowing, for instance, some error of metabolism. This would be 
caused, for example, by the presence in the stomach of an in- 
sufficient amount of hydrochloric acid (hypochlorhydria). From 
the physician's standpoint hypochlorhydria is the exciting or 
direct cause of the digestive disorder to which it has given rise, 
while from the dentist's standpoint, hypochlorhydria is only the 
predisposing cause of the dental disorder, for the reason that it 
has brought about errors of metabolism which prevent the de- 
velopment of a sufficient degree of vital resistance in the in- 
vesting tissues of the teeth and retard or prevent the eradication 
of the infectious processes around the teeth. Any systemic con- 



216 DENTAL PATHOLOGY 

dition which is a deviation from the normal, and which is the 
result of a combination of exciting causes, may become the pre- 
disposing cause of a dental or oral disease. 

Disease, general or dental, itself is not a separate entity, out may 
be defined as abnormality in structure, in function, or in both com- 
bined} 

The general division of disease into organic and functional, im- 
plying in the former case alteration of cellular structure, and 
in the latter alteration of physiologic function without alteration 
of structure, is of doubtful value in its application to general dis- 
ease and to dental and oral disease. It is true that physiologic 
derangement may exist without any apparent structural changes, 
but then it is more probable that cellular changes have taken 
place which it is not possible to locate and analyze because of 
as yet a relatively imperfect pathologic technic. The conception 
of modern pathology, general and dental, is almost exclusively 
anatomic, i.e., structural changes in the cells. The changed ap- 
pearance of an organ which results from the changes in its cells; 
the study of the retrograde changes in the cells themselves by 
means of the microscope ; the changes in the body secretions ; the 
nature of the body excretions — these are some of the most im- 
portant phases in the study of pathology, whether general or 
dental. Gross pathology studies macroscopic changes only. 

Prior to the promulgation of the cell theory of disease, the 
study of pathology consisted almost exclusively in the observa- 
tion of gross anatomic changes, and in the manifestations of 
pathologic physiology. The conclusion that disease is the result 
of the sum total of the changes which take place in the individual 
cells consequent upon the continued influence of irritation, ab- 
normal in character or amount, marks the beginning of a logical 
conception of general and dental pathology. 



'Stengel and Fox: Text-book of Pathology, Philadelphia, W. B. Saunders. 



CHAPTER XI 
ENAMEL, DENTIN, AND CEMENTUM 

Normal Histologic Considerations 

It being impossible to appreciate deviations in the substance 
of the enamel, dentin, or cementum,— the hard tissues of the 
teeth — in the pulp, or in the bony or soft investing structures, 
without previous clear conceptions of these tissues when within 
the limits of normality, it becomes advisable to review the his- 
tology of all of them beginning with that of the enamel. We 
shall consider also the relation of the latter to the dentin and 
cementum, bearing in mind that the study of the normal charac- 
teristics of these tissues is undertaken as a means of facilitating 
the comprehension of the pathologic processes which may con- 
cern them. 

Normal Enamel 

The enamel, the hardest tissue of the body, is a specialized 
form of calcified epithelial tissue of ectodermic origin, which 
surrounds the crown of the tooth in its entirety and extends to 
the gingival line. Here it is covered by the unattached gingiva 1 
for a distance of several millimeters. It varies in thickness from 
the gingival line, where it is the thinnest, to the occlusal or in- 
cising edges where it is the thickest. The increase in thickness 
is gradual and particularly well marked at such areas of the 
tooth as are usually subjected to strong and continued friction and 
stress during mastication. The greater the stress to which an area 
of crown surface is subjected, the thicker and more resistant will 
be the enamel on such an area, not because of any difference in 
chemical composition, but because of a peculiar arrangement of 
the enamel rods to meet the requirements of great stress. Per- 
fection in development throughout the enamel is rarely encoun- 
tered so that in describing this tissue our aim will be to describe 
the microscopic appearance of an average specimen falling within 
the limits of normality. (Figs. 88 and 89.) 

217 



218 



DENTAL PATHOLOGY 




Fig. 88. — Area of normal dentin and enamel, a, dentin; b, enamel; c, c' , dentoenamel 
junction; c, dentinal tubuli; f, series of interglobular spaces faintly reproduced. 



EXAAIEL, DEXTIX, AXD CEMEXTUM 



219 



The components of enamel are the enamel rods and the cement- 
ing or inter prismatic suostance, the latter being the binding ma- 
terial which holds the rods together. This substance, like the 
enamel rods, of ectodermic origin, is a calcined stratified-squa- 
mous epithelium. The rods are five- or six-sided and from three 
and one-half to four and one-half microns in length. Some of 
the rods may be traced from the dentoenamel junction to the 
surface of the crown of the tooth. The cementing' substance is 




Fig. 89. — Area of normal dentin and enamel from ground section of area near apex 
of incisor of man. a, dentin, showing dentinal tubules; b, enamel; c, crack in enamel 
made in grinding. 



more susceptible to the action of dilute acids than the enamel 
rods, so that if a section of enamel be subjected to dilute hy- 
drochloric or lactic acid, until the cementing substance is in part 
dissolved, a clear differentiation between enamel rods and ce- 
menting substance will be obtained. This is due to the fact 
that upon the removal of the cementing substance a greater dif- 
ference in the indices of refraction of the enamel rods and the 
decreased cementing substance between them will have been es- 



220 



DENTAL PATHOLOGY 



tablished (Fig. 90). Examination of a ground section of a tooth 
with a 16 mm. objective does not render possible the detection 
of the physical peculiarities of the individual rods or of the ce- 
menting substance. With a higher magnification, in a longi- 
tudinal section the individual rods appear as a series of striations 
of alternating dark and light areas. It is with difficulty that a 
rod can be traced microscopically from its free end to the dento- 
enamel junction. Upon the axial surfaces the rods are more or 
less parallel to each other and most of them, according to Noyes, 
extend from the dentin to the free surface of the enamel. 1 That 



ppi 



.__& 



Fig. 90. — Contrast between normal enamel at a and a', and decalcified enamel at b and b' . 

they extend as single rods to the free surface of the enamel must 
be concluded largely from observation in cleaving enamel in 
the preparation of cavities for the reception of fillings. Mi- 
croscopically it is practically futile to attempt to trace the rods 
across the section as single rods. The majority of sections that 
have been examined by the author show the tendency toward 
parallelism of the rods on the axial surfaces, but, on the other 
hand, do not show many rods traceable uninterruptedly from 
within to the free surface of the enamel (Fig. 91). 

^oyes: Dental Histology and Embryology, Philadelphia, Lea & Febiger. 



ENAMEL, DENTIN, AND CEMENTUM 



221 



Another peculiarity of enamel, within the bounds of nor- 
mality are the lands of Retzius. These are better seen upon ex- 
amination with a low-power objective and appear as brownish 
striations which mark the beginning and completion of the cal- 
cification of sections of enamel structure. They are the boundary 
lines between calcification installments, and hence have been ap- 
propriately named by the descriptive term incremental lines 



a 




Fig. 91. — Ground section. Dentoenamel junction. The character of the granular 
layer of Tomes is unusually well shown. The bearing which this layer has upon the 
progress of caries should not be overlooked. This section also shows the tendency at 
parallelism of the enamel rods; a, a', enamel; b,b', dentin; c,c', granular layer. 

(Noyes). The portions of enamel included between the dento- 
enamel junction and a band of Retzius, and between the bands 
themselves, represent synchronous calcification installments (Fig. 
92). These bands of brownish color, when viewed under a low 
or high amplification, run obliquely across the lengths of the 
enamel rods from the dentoenamel junction on one side to the 



222 



DENTAL PATHOLOGY 



dentoenamel junction on the opposite (from mesial to distal sur- 
faces) in the incisal region and in the cusps of bicuspids and 
molars. Beyond these regions they run from the dentoenamel 
junction to the surface of the enamel. They mark the strata of 
enamel in the order of their calcification. They begin at the 
dentoenamel junction in the region of the incisal area, and ter- 

d 



d' 



I 

I 



Fig. 92. — Ground section, longitudinal, showing the prevailing mode of junction of 
enamel and cementum. Inasmuch as the calcification of the enamel is completed before 
that of the cementum begins, the latter tissue either overlaps the enamel or the joint is 
of the butt type. The lines of Retzius are also seen, a, a', dentin; b, b' , enamel; c, c' , 
cementum. In the enamel the lines running obliquely from the dentin to the free sur- 
face of the enamel are the lines of Retzius d, d' ; line of junction between enamel and 
cementum, the latter overlapping the enamel, seen at c. 

minate, after following a curved course, at some other point in the 
dentoenamel junction. 

Sections of enamel when examined under a low power with 
direct light occasionally exhibit markings or bands running at 
right angles to the dentin. These are the lines of Slireger and 
are due to "alternating uniform curvatures of the prismatic 



ENAMEL, DENTIN, AND CEMENTTJM 223 

bundles." They embody no significance, histologic and path- 
ologic. 

Eecently Lodge 2 has made an interesting study of the cause of 
the presence of these lines. He has found, by superimposing two 
wire screens and viewing them over a white surface or by sub- 
dued transmitted light or by placing together two layers of a 
silk fabric, that the lines of Shreger can be simulated. The lines 
of Shreger are due, according to Lodge, to "net" effects pro- 
duced by light falling upon the cut enamel prisms, the optical 
densities varying according as the meshes of these nets are in 
apposition or in interference. The lines are difficult to see where 
the section is cut absolutely parallel to the long axis of the 
enamel rods, but are plainly observable when sections of the 
same enamel are made at 45° or more to the first-made sections. 

Chemically, the enamel is composed mainly of salts of calcium, 
with a trace of salts of magnesium, and other salts in smaller 
proportions. This may be outlined as follows : 



Calcium phosphate and 


fluoride 


89.82% 


Calcium carbonate 




4.37% 


Magnesium phosphate 




1.34% 


Other salts 




.88% 


Organic matter 




3.59% 




100% 



It possesses a peculiar luster, to which it owes its names. The 
word enamel is derived from the old French word csmail, this in 
turn being derived from the Latin smalium, a term first given to 
a vitreous compound when fused upon a metallic surface. 

The surfaces of the enamel upon all the aspects of the tooth 
are not normally smooth, but on the contrary the enamel is 
"traversed on its vertical aspect by minute ridges separated 
from each other by corresponding 'furrows' which run parallel 
to each other in a direction at right angles to the long axis of 
the tooth. These horizontal lines are in some cases large enough 
to be visible to the naked eye, and must have been noticed oc- 
casionally by many who, like myself [Pickerill] , thought at first 
that they were either caused by attrition or were a microscopic 
form of hypoplasia." 3 



2 Lodge, E. Ballard: Dental Cosmos, lix, 1087. 

3 Pickerill: The Prevention of Dental Caries and Oral Sepsis, Philadelphia, S. S. 
White & Co, 



224 



DENTAL PATHOLOGY 



This investigator has named these horizontal lines "the imbri- 
cation lines of the enamel" (Figs. 93 and 94). These horizontal 
lines are widest and the furrows between them deepest at a 




Fig. 93. — Imbrication lines on lower incisor of sclerotic type (Pickerill.) 







Fig. 94. — Imbrication lines on lower incisor of malacotic type (Pickerill.) 

point two-thirds the distance from the neck of the tooth to the 
cutting or occlusal surface. In the teeth of the uncivilized races 
in which dental caries is so much less frequent than in the teeth 
of the modern races, the imbrication lines are less marked. In 



ENAMEL, DENTIN, AXD CEMENTUM 225 

fact, lie says, the enamel of the teeth of the primitive races is 
more lustrous, and the imbrication lines are so feeble that they 
can not be brought out by the graphite method of staining. In- 
asmuch as the more susceptible to caries a tooth is, the more 
marked are the imbrication lines and the deeper are the fur- 
rows between them, the conclusion is reached that the character 
of the external surface of the enamel as to the presence of mi- 
croscopic and macroscopic unevennesses is one among many factors 
which determines the susceptibility of the tooth to dental caries. The 
less smooth the surface of the enamel, the more difficult it be- 
comes to maintain these surfaces free from food deposits, saliva 



Fig. 95. — Calcarine fissures on the surface of a malacotic molar (Pickerill). 

or salivary mucin. In addition to these imbrication lines upon 
the surface of the enamel which are apparently external mani- 
festations of the thickness, the uneven lengths and number 
of the bands of Eetzius, the enamel also presents fissures which 
are short and numerous, and which run more or less at right 
angles to the horizontal imbrication lines. These should be des- 
ignated as "Pickerill's calcarine fissures.' ' They are present in 
greatest numbers on the mesial and distal surfaces and on those 
points where the ridges are most marked, i.e., at a point one-half 
the distance between the cervix and the occlusal surface (Fig. 
95) . Shallow long fissures and deep fissures' which may run either 
parallel with or at right angles from the long axis of the tooth, 



226 DENTAL PATHOLOGY 

are also present in the teeth of the modern races susceptible to 
dental caries and are etiologic factors in the frequency of caries 
in these races; and vice versa, their absence from the enamel 
of the teeth of the primitive races accounts to some extent for 
their nonsusceptibility to caries. 

The question of the comparative hardness of teeth has been for 
many years the subject of contradictory conclusions on the part 
of investigators and clinicians, the latter tenaciously adhering to 
the observations that from the standpoint of resistance to the 
cutting edge of instruments or to the revolving dental bur, the 
enamel and dentin in different teeth in the same mouth, or in 
different mouths, are not of the same degree of hardness. The 
conclusions of G. V. Black 4 are that the clinicians' classification 
of teeth into hard and soft is untenable in the light of his 
findings on the calcium salt content of teeth which decay badly, 
and of those which are immune to caries. He says that "teeth 
that decay badly have just as much calcium salts, are just as 
heavy and just as hard as teeth of persons immune to caries," 
but this must be modified to some extent on the face of the find- 
ings and conclusions of Pickerill. In order to secure a clear idea 
of the position assumed by the latter investigator, it becomes nec- 
essary to establish a difference between the specific gravity of the 
enamel and its mass density. The fact that from any number 
of specimens the enamel is of the same specific gravity, is no 
guarantee that the mass density of the different specimens is 
likewise unvarying. The specific gravity of individual enamel 
rods may be the same, but the mass density of the caps of enamel 
seems to vary as between teeth which decay readily and those 
which do not. Thus the mass density of the enamel of "native" 
teeth (teeth of the uncivilized tribes least susceptible of all to 
the ravages of caries) was found to be 2.858; that of so-called 
hard (sclerotic teeth), 2.821; and that of so-called soft (malacotic) 
teeth, 2.723. 5 These differences in density are apparently due to 
differences in the porosity of the enamel even in the presence of 
an unvarying specific gravity of individual enamel rods or groups 
of rods. The differences in porosity account for the various 
degrees of permeability of the enamel at different ages in the 



4 Black, G. V.: Dental Cosmos, xxxvii, 353. 
5 Pickerill: Loc. cit. 



ENAMEL, DENTIN, AND CEMENTTJM 



227 



same teeth and in teeth, from different mouths. Thus, as re- 
corded by Pickerill, the permeability of the enamel decreases 
with the age of the tooth; or, the shorter the time elapsed since 
the day of eruption, the more permeable the tooth, and vice 
versa. Likewise, the less the age of the tooth, the smaller is its 
mass density; and the greater the age of the tooth, the greater is 





Fig. 96. — Decalcified longitudinal section showing butt type of enamel-cementum 
junction at a. Some of the enamel rods at b are seen to run uninterruptedly from the 
dentoenamel junction to the free surface. The primary curves of the dentinal tubules 
at the dentoenamel junction carry out the arrangement so frequently prevailing, viz., the 
convex outline of the curvature is toward the root, and the concave toward the incisal or 
occlusal surface. 



its mass density. Pickerill sees a direct relation between the per- 
meability of the enamel and the effects of acids. In fact the com- 
parative tests show greatest destructiveness by acids in just those 
teeth and at just such times as the porosity of the enamel is most 
marked and the density proportionately less marked. 



228 DENTAL PATHOLOGY 

The unvarying hardness of the enamel of all teeth — one of 
Black's conclusions — is likewise questioned by Pickerill on the 
basis that the more reliable methods of determining the hardness 
of various substances by scratching were not then employed. 
Pickerill has used in these experiments an ingenious device of 
his invention, the sclerometer, by means of which "the tooth 
to be examined is made to glide under a diamond point which is 
attached to an accurately balanced brass rod. The rod beyond 
the point is graduated in centimeters and millimeters, and on 
the rod slides a 5- or 10-gram weight. By altering the position 
of the weight on the rod, an increasing amount of pressure can 
be made on the diamond point; and since the weight is known 
and the distance is known, it is a simple matter to calculate the 
actual pressure upon the point for any setting. The method 
adopted was to draw the tooth under the point with gradually 
increasing pressures until in the enamel a scratch was made which 
could be distinctly seen with the naked eye when rubbed with 
graphite. A series of teeth examined in this way by the same 
observer, with the same diamond point and at the same time 
of day, supports his contention that there is a difference in the 
hardness of different enamels, and that this difference exists be- 
tween so-called hard (sclerotic) teeth, and soft (malacotic) 
teeth." 

The line of junction between the enamel and the cementum 
is either one in which the cementum overlaps the enamel (Fig. 92) 
or else one in which the two tissues form a butt joint (Fig. 96). 

Dentin 

The dentin forms the bulk of the tooth (Fig. 97) being covered 
by the enamel in the crown portion of the tooth and by cementum 
in the root portion. Even after the removal of the enamel, the 
outlines of the mass of dentin follow the general shape of the 
crown and root of the tooth. It is a specialized form of cal- 
cified connective tissue of mesodermic origin — a glue-giving sub- 
stance — composed of minute channels, the dentinal tubules, from 
1.3 to 2.5 microns in diameter (Figs. 98 and 99), these containing 
the dentinal fibrillce which are the protoplasmic prolongations of 



°From the pathologic standpoint the investigations of Pickerill on the physical and 
chemical properties of human enamel are of untold value; for a complete survey of the 
question the reader is referred to the original work. (Pickerill, II. P.: Loc. cit.) 




Fig. 97. — Longitudinal section of upper cuspid showing the course and arrangement 
of the dentinal tubuli. The arrangement of the enamel rods and the anastomosis of the 
tubuli at the dentoenamel junction are seen. This picture is from a pen and ink drawing 
of a ground section which did not involve the root canal in its entirety. 



ENAMEL, DENTIN, AND CEMENTUM 



229 




Fig. 98. — A field of dentinal tubules. At a, b. and c individual tubules are plainly visible. 




Fig. 99. — Transverse section of dentin. The dentinal tubules are cut somewhat diagonally, 



230 DENTAL PATHOLOGY 

the odontoblastic layer of the pulp; of a matrix, the dentin matrix, 
or substance occupying the spaces between the tubules ; and of the 
sheaths of Newman, which may be sheaths of the fibrillar lying in 
apposition with the tubular wall or a substance more resisting 
to acids than the dentin matrix, and located immediately outside 
the tubuli. The substance which makes up the sheaths of New- 
man is probably elastki, soluble only in concentrated acids or 
caustic alkalies, but digestible by bacterial ferments. 

Dentin is hard, though elastic, usually of a yellowish white 
color and of a slight degree of translucency. In the crown por- 
tion of the dentin the tubuli run a wavy course from the dento- 
enamel junction to the walls of the pulp chamber, and being 
disposed everywhere in a more or less perpendicular direction 
to the external surface of the tooth, radiate in various directions. 
In the root portion of the dentin they run for a distance only, 
an almost straight course at practically right angles to the long 
axis of the tooth, but as the apical third of the root is approached, 
their direction becomes apical and a radial effect is produced. 
The diameter of the tubules is greater on the pulp end than on 
the enamel or cementum end and are in closer proximity to each 
other where they are the wider in diameter. The tubules anas- 
tomose with one another, these anastomoses being more marked 
in the root than in the crown. In the incisors, in the middle of 
the incisal region of the crown, the tubules run a course almost 
parallel with the long nxis of the tooth, maintaining this for a 
short distance toward the mesio-incisal and disto-incisal angles. 
They then assume a course which becomes less and less oblique, 
until the junction of the lower with the middle third of the root, 
where the course of the tubules is practically at right angles to 
the long axis of the tooth. The tubules follow the same relative 
direction upon the labial and lingual and mesial and distal as- 
pects of the tooth in its entire length. In the incisal region, if 
a mesiodistal section be examined, the tubuli will be found to 
run from the dentoenamel junction toward the pulp chamber in 
a fan-like arrangement. 

In molars and bicuspids the tubules form an arrangement 
something like this: Beginning at the enamel-cementum junction 
and toward the occlusal aspect the tubules sweep toward the pulp 
chamber describing a double curve. The curve near the dento- 



ENAMEL, DENTIN, AND CEMENTUM 



231 



enamel junction presents its convex surface toward the occlusal 
and its concave surface toward the apex. The curve at the root 
canal wall is less marked, the concave aspect being directed 
toward the occlusal and the convex toward the apex. The tubules 
in relation to the cusp present a typical wheat-sheaf arrangement. 
The granular layer of Tomes, so-called because of its having been 




Fig. 100. — Interglobular spaces ot Czermack in the dentin. Evidences of periods of 
arrestment of calcification of the dentinal tubules. The presence of a large number of 
these spaces would render more rapid the progress of caries in the areas in which they 
are located, by reason of the greater penetrability of the tissue to the acid end products 
of fermentation, a, a' , a", interglobular spaces of Czermack. 



first described by Sir John Tomes, represents a system of inter- 
communication among the tubules at the dentin-cementum and 
dentoenamel lines. It is more marked at the dentin-cementum 
line than it is in the crown portion of the tooth. These spaces, 
produced by the widening out of the tubules, are filled with pro- 
toplasmic matter and are responsible for the increased sensitive- 



232 



DENTAL PATHOLOGY 



iiess of dentin in these areas. Into the spaces of the granular layer 
in the root or crown portions of the tooth the tubules empty, so 
to speak, and in some instances they have been observed to pass 
beyond for some distance into the cementum and the enamel. 
Practically every specimen of enamel shows that here and there 
dentinal tubules penetrate its substance for a clearly perceptible 
distance, a condition which may render very much less unreasona- 
ble the observed fact that occasionally teeth are encountered 
where enamel responds to stimuli. 




Fig. 101.— -Longitudinal ground section of tooth showing fields of dentin at a, a' and 
enamel at b, b' . " In the body of the dentin at some distance from the dentoenamel 
junction and the granular layer at c, c' large numbers of interglobular spaces are seen 
at d, d'. 

The granular layer of Tomes should not be confused with the 
interglobular spaces (Figs. 100 and 101), which are located in the 
body of the dentin at some distance from the granular layer. 
These spaces are more marked in the crown portion of the dentin 
and in the gingival third of the root, and are, beyond certain 
limits, evidences of hypoplastic phenomena (imperfect develop- 
ment) of the dentin matrix and dentinal tubules. They are 
plainly visible in ground sections with a high or low power. 



ENAMEL, DENTIN, AND CEMENTUM 233 

In fresh specimens they are filled with calcified or semi-calcified 
dentin matrix, or protoplasm. A few tnbnles may pass through 
the space. In old specimens the spaces appear dark, being filled 
with debris from the grinding process. They have been called 
interglobular spaces, (i. e., spaces between globules) for the rea- 
son that similar outlines can be made by zones of spheres. 

AVithin certain limits as to size and number, the interglobular 
spaces may be considered as not abnormal characteristics of den- 
tin. Every specimen of dentin, however, is, strictly speaking, not 
a normal one if considered from the standpoint of the inter- 
globular spaces, for these must be viewed as evidences of tem- 
porary arrestments of development. 

The chemical composition of dentin may be outlined as fol- 
lows : 

Calcium phosphate, 66% 

Calcium carbonate, 3 to 4% 

Magnesium phosphate, 1 to 2% 

Organic matter, 27 to 28% 

" 100% 

Cementum 

It is that bone-like tissue which envelops the root of the tooth in 
its entirety and which, beginning as a slender covering at the 
enamel line, gradually increases in thickness until the apical re- 
gion is reached, where it is the thickest. The cementum is de- 
veloped from the fibrous envelope of the tooth follicle — the so- 
called follicular wall. It differs from bone in that it does not 
contain any Haversian systems; in that it possesses no blood or 
nerve supply of its own, but depends exclusively for its nutrition 
and innervation upon the peridental membrane; and in that from 
the pathological standpoint, it has no reparative power, except 
in so far as this occurs through the agency of the peridental mem- 
brane. The cementum is deposited in layers, the deposition of 
a new layer not beginning until the previous one is completely 
calcified. These layers, or lamcllce, are distinguishable under Ioav 
and high amplifications and represent the incremental lines of 
the cementum (Figs. 102 and 103). Within its substances are 
found the lacunce or spaces containing active cells from the follic- 
ular wall — the cement oblasts, which became encapsulated during 
the calcification process. From the lacunae a considerable num- 



!34 



DENTAL PATHOLOGY 



ber of small canals lead out, and these communicate with similar 
small canals from other lacunas. These small canals are the 
canaliculi and they, as well as the lacunce, as has been stated, are in 
healthy cementum filled with protoplasmic matter (Fig. 104). 

The matrix is granular in some locations and fibrous in others. 
In decalcified specimens in which the organic portion of the ce- 
mentum is adherent to the dentin, the fibrous character of the ma- 
trix is plainly visible in some localities. As the cementum calcifies, 







1 









Fig. 102. — Transverse ground section at the apical region of a root. In the apical 
region and in root bifurcations and trifurcations the cementum is the thickest. The 
lamellae or layers of cementum may here he seen especially at a; the dentin at b; and 
the root canal at c. 



through the agency of the cementoblasts in the peridental-mem- 
brane-to-be, some of the fibers of the latter tissue in its em- 
bryonic stage become encased in the cementum (Fig. 105). They 
are to be found, as seen in Fig. 105, not in proximity to the 
granular layer, but at some distance therefrom in cementum rather 
younger in development. The similarity in development between 
cementum and subperiosteal bone lends credence to our belief 
that the fibrous appearance of the cementum matrix is due to 



EXAVLEL, dextix, axd cemextum 



235 



the deposition of inorganic salts in a fibrous framework, and 
also to the fact that wherever calcification is not carried on 
to full completion the semicalcified fibers persist as such. These 
fibers bear to cementum the same relationship in genesis as Shar- 
pey's fibers do to bone. 

The lacuna? of variable size and shape are practically absent 
in the thin portion of the cementum (Figs. 106 and 107), but are to 




Fig. 103. — Transverse ground section of tooth at the heginning of apical third of 
root. Observe that here the thickness of cementum is markedly less than what it is 
farther apically. a, a' lamelhe of cementum; b, dentin; c, root canal. 

be found in considerable numbers wherever the cementum is 
thick and in hypercementosis. They are located in areas nearer 
the dentin, as shown in Fig. 108, but may also be found equidis- 
tant from the granular layer and the external cementum surface 
(Fig. 109). The lacuna? are particularly abundant in the apical 
region and in the bifurcations and trifurcations of molars (Fig. 
110). The layers of cementum next to the peridental membrane 
and those next to the dentin as a general rule contain fewer 



236 



DENTAL PATHOLOGY 



lacunae than those in the central portion. In hypercementozed 
specimens the lacunae are distributed throughout the tissue with- 
out regard to form, number, or arrangement. The tissue is 



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Fig. 104.— Thick area of ccmcntum in the bifurcation of the roots of a molar, showing 
lacuna? and canaliculi and intercommunication of canaliculi. 



characterized, however, by the presence of large numbers of 
lacunae. The form and size of the lacunae vary within certain 
limits in the same tooth, and the canaliculi branch out in 



ENAMEL, DENTIN, AND CEMENTUM 237 

every direction, although principally toward the peridental mem- 
brane rather than toward the dentin. 

Dentinal tubules here and there penetrate into the cementum 
for some distance and anastomose with the canaliculi of the 
lacuna*. It is a difficult matter, however, to see this arrangement 
even with the highest power of the microscope in all cases, but 
the author has seen it in a sufficient number of cases to warrant 
him in believing that such is the case, and that if it can not 
a e b' 



Fig. 105. — Longitudinal ground section showing at a dentin, at b, b' clear, glossy, 
so-called hyaline cementum and at c, a more recent cementum formation than at b, in 
which intraalveolar fibers of the peridental membrane appear encapsulated in the cementum 
and at d some few lacunae with their respective canaliculi. At c, c' the granular layer 
is seen. 

be demonstrated in all cases it is not because the dentinal tubules 
and canaliculi do not communicate, but rather because mi- 
croscopes are not sufficiently powerful to demonstrate it. As 
to whether or not a system of nutrition is thus established 
to the cementum from the dentin, and to the dentin from, the 
cementum, is as yet an unsolved problem in dental physiology. 
There are those who believe that such is the case, but. convincing 
proof thereof is as yet lacking. 7 E. R. Andrews believes that in 



r Choquet: Precis D'Anatomie Dentaire. 




Fig. 106. — Ground section, longitudinal, showing gingival third of root. The cementnm 
appears devoid of lacunae. The darker lines running at right angles with the tubuli are 
artifacts — cracks in the specimen caused by shrinkage in drying, Idled with air and pow- 
dered tooth substance from grinding. 




Fig. 107. — Ground section, longitudinal, showing 
and canaliculi, a, a', dentin; b, b' , hyaline cementum. 



ttum devoid of lacuna: 



ENAMEL, DENTIN, AND CEMENTUM 
a b 



239 



Fig. 108. — Longitudinal ground section of cementum showing lacuna: in areas near 
dentin at a; fibers of peridental membrane incased in the cementum at b. The granu- 
lar layer is seen at c; the width of cementum is from d, d'. 




Fig. 109.- — Longitudinal ground section in gingival third showing at a, lacunae and canal- 
iculi equidistant from granular layer at b, b' , and external cementum surface at <r. 



240 



DENTAL PATHOLOGY 



the fully formed cementum the processes of the cementum cor- 
puscles undoubtedly anastomose with those of the peridental 
membrane, with each other, and with the processes of the granu- 
lar layer just within the dentin. 8 




Fig. 110. — The cementum in the apical region of the roots of an upper first bicuspid. 
The section did not involve the root canal. The dark spots represent the lacunae. 

The chemical composition of cementum according to von Bibra 
is as follows : 



Calcium phosphate, 


48.73% 


Calcium carbonate, 


7.22% 


Magnesium phosphate, 


0.99% 


Soluble salts, 


0.82% 


Organic matter, 


42.24% 



100.00% 

If this analysis is compared to that of bone, it will be seen 
that cementum contains 18.90 per cent more organic matter than 
bone, and 8.94 per cent less inorganic matter. 



8 Andrews, R. R.: Calcification, Dental Cosmos, January, 1912. 



CHAPTER XII 

DEVELOPMENT OF THE TEETH 

From the fiftieth to the sixtieth day of intrauterine life the first 
step in the development of the teeth becomes evident. At this time 
a thickening of the stratum malpighii of the oral epithelium along 
the peripheral area of the jaws is to be observed. This thickening 
of the oral epithelium progresses in the direction of the under- 
lying connective tissue and constitutes the dental band or ridge 
(Figs. Ill and 112). The dented groove, a term frequently en- 
countered in connection with the embryology of the teeth, can 
refer only to the appearance of a transverse vertical section of 
a developing jaw where it Avill be seen that the underlying con- 
nective tissue has been scooped out, so to speak, the groove be- 
ing filled with masses of epithelial cells — the epithelial band — a 
term which more accurately describes the early stages of tooth 
embryology than the term dental ridge. If we picture, as sug- 
gested by Magitot, 1 a rope of epithelial cells snugly fitting into 
a depression in the connective tissue, it will facilitate a correct 
conception of the dental band and dental groove, the band being 
the epithelial rope and the dental groove being the grooved bed 
in which the rope rests. The dental band is convex externally 
and concave internally. From the concave surface, about mid- 
way between the apex and the base of the band, an epithelial pro- 
jection — the dental lamina — grows out lingually almost at right 
angles to the vertical diameter of the band. This projection does 
not occur at any one particular locality, but extends along the 
entire length of the band. A shelf growing out at right angles 
to the band will explain better the relationship of the dental 
lamina to the dental band. 

From each of twelve points on the dental lamina, in each jaw, 
an epithelial cord grows out, at first in a horizontal direction to- 



1 L,egros, Ch., and Magitot, K.: Dental Follicle. 

241 



242 



DENTAL PATHOLOGY 



ward the lingual aspect of the primitive jaw, and then in a di- 
rection almost at right angles from the lamina. Of these cords, 
the anterior ten are destined to form the enamel organs of the de- 
ciduous teeth, and the posterior two, those of the permanent first 
molars, of each arch. The epithelial cord is composed of epithe- 




• 'VXr 




Fig. 111. — First evidence of tooth development. The stratified squamous epithelium is 
seen dipping into the subadjacent connective tissue and forming the dental band or ridge. 
a, epithelial hand progressing in the direction of the underlying connective tissue; b, b' , 
and b" , thickened epithelial layer; c, underlying connective tissue. 



DEVELOPMENT OF THE TEETH 



243 



lial cells from the lamina, and the latter, in turn, from the periph- 
eral cells of the dental band. As each epithelial cord, which 
is an outgrowth of the dental lamina, proceeds downward and 
somewhat lingually, and after obtaining a certain length, it un- 
dergoes characteristic changes which materialize about the ninth 




_ Fig 112.— A slightly later stage than in the preceding illustration showing the begin- 
ning of the invagination of the epithelial cord which will result in the formation of the 
tour layers of the enamel organ, a, epithelial cells from the more superficial or older 
strata of the Malpighian layer; b, younger strata from Malpighian laver from which 
dipping of epithelium occurs; c, epithelial cord beginning to undergo the invagination 
which will result m the formation of the four distinct groups of cells of the enamel or- 
gan; a, condensation of underlying connective tissue. 



244 



DENTAL PATHOLOGY 



week of embryonal life. These changes result in the eventual 
formation of the enamel organ. 

There occurs an upward invagination in the case of the lower 
enamel organs, and a downward invagination in the upper, which 
progresses until a hood-shaped organ has resulted which sur- 
rounds a condensation of connective tissue cells (the dentin-forming 
organ, or dental papilla). The enamel organ as now constituted 



* , ,;, 




Fig. 113. — The four sets of cells of the enamel organ; a, the internal or the layer of 
the ameloblasts; b, cells of the stratum intermedium; c, cells of the stellate reticulum, 
and d, of the external layer. Portions of the follicular sac are seen at c, surrounding 
the dental papilla and enamel organ; from the follicular wall the cementum and alveolar 
process will develop. 



will consist of an external layer of epithelial cells ; of an internal 
layer, which is formed from the invagination of the outer layer of 
the enamel bud ; of a layer of cells in close contact with the inner 
aspect of the internal layer — the stratum intermedium; and of 
a number of stellate cells occupying the space between the external 
and internal layers — the stellate reticulum (Fig. 113). The stra- 
tum intermedium and the stellate reticulum originate from the 
inner cells of the dental lamina, and these in turn from the inner 



DEVELOPMENT OF THE TEETH 245 

cells of the dental band. The internal layer consists of the 
enamel building cells ameloblasts, or enameloblasts ; the external 
layer begins to show signs of an atrophic process prior to the 
completion of the enamel; and the cells of the stratum inter- 
medium and those of the stellate reticulum are probably concerned 
in supplying the ameloblasts with such nutritional elements as 
are required by them during enamel formation. In other words, 
and to present a mental sketch of the germ, the enamel or- 
gan is a double hood containing between the external hood and 
the internal hood the cells of the stratum intermedium and stel- 
late reticulum, the double hood enclosing a specialized mass of 
embryonal connective tissue cells — the dental papilla, or dent in- 
forming organ. For a time the enamel organ remains connected 
to the dental lamina by means of a slender cord of epithelial cells 
designated as the epithelial cord. It gradually atrophies, and by 
the time the thirteenth week of embryonal life has been reached, 
the cord is ruptured and the tooth follicle proceeds in its de- 
velopmental work independent of any connection with the oral 
epithelium. 

The enamel organ of all the deciduous teeth may be said to ap- 
pear about the eighth week of embryonic life; the dental papilla 
about the ninth week; the follicular wall which encircles the 
tooth follicle, (i.e., enamel organ and dental papilla), rises from 
the base of the dental papilla and appears at the tenth week; 
the follicle closure and simultaneous rupture of the cord occurs 
about the thirteenth week; and the formation of dentin begins 
about the sixteenth week. 2 

The enamel buds of the permanent teeth, with the exception of 
the first, second and third molars, begin to develop about the 
sixteenth week from the epithelial cord of the corresponding 
temporary tooth, the process of development being analogous to 
that of the temporary teeth. The first molars develop from in- 
dependent invaginations of the dental ridge about the fifteenth 
week of intrauterine life in exactly the same way as do the de- 
ciduous teeth (see above) ; the second molars develop from an 
offshoot of the epithelial cord of the first molar, about the third 



2 Legros, Ch , and Magitot, E. : Chronology of the Dental Follicle in Man. Ti 
lation by M. S. Dean. 



246 DENTAL PATHOLOGY 

month after birth; and the third molars develop from offshoots 
of the second molar, about the second or third year after birth. 

The calcification of the enamel proceeds from within outwards, 
while that of the dentin from without inwards. A divergence of 
opinion exists in regard to the process by which enamel is cal- 
cified, particularly so concerning the ultimate fate of the cells 
of the enamel organ. Aside from the facts that the internal 
epithelial layer of the enamel organ is the enamel-building layer ; 
that the cells of the stratum intermedium are probably substitu- 
tion enamel cells (i.e., they replace functionally exhausted amelo- 
blasts) ; and that the cells of the stellate reticulum are the agen- 
cies of nourishment to the active enamel-building cells — nothing- 
based upon actual observations has so far been brought out that 
could be considered otherwise than as mere theories. The amelo- 
blasts are elongated cells which become more or less hexagonal 
by mutual apposition. 3 They are in close relation to the large 
round cells of the stratum intermedium. The cells of the stellate 
reticulum are connected among themselves by means of processes, 
a reticulated appearance being the result. The cells of the ex- 
ternal layer, after the cells of the stellate reticulum have atro- 
phied, coalesce with those of the internal layer and persist for 
some time after the eruption of the teeth as Nasmyth's membrane. 
The enamel begins to form on the deciduous teeth about the seven- 
teenth week of embryonic life, ending about the sixth month after 
birth. On the permanent teeth it begins to form at birth or 
slightly before birth, and ends about the twelfth year on the crown 
of the third molar. 1 

Dentin 

As has been previously noted, the dental papilla, or dentin- form- 
ing organ, makes its appearance about the ninth Aveek, or ap- 
proximately a few days after the beginning of the formation of 
the dental groove by the inward growth of the dental band. 
The dental papilla (dentin-forming organ, dental bulb) is a mass 
of embryonal connective-tissue cells (Fig. 114), whose peripheral 
cells assume a quasicolumnar shape and arrange themselves in 
a fairly regular way. The cells have a well-defined nucleus 



3 Tomes: Dental Anatomy, Philadelphia, P. Blakiston's Son & Co. 
4 Andrews, R. R. : Dental Cosmos, 1912. 



DEVELOPMENT OF THE TEETH 



247 



occupying a position in the internal third of the cell toward the 
dental papilla, and differ in appearance as to whether dentin is 
being actively produced or not. During active dentinification 
the ends of the odontoblasts next the alreadv formed dentin are 




Fig. 114. — Same stage of development as seen in the preceding illustration. The fol- 
licular sac which springs from the base of the dental papilla is seen surrounding the de- 
veloping organ. a, follicular wall; b, dental papilla; c, internal or ameloblastic layer. 

expanded; at periods of arrested deiitinification the cells seem 
longer and their ends more slender and rounded. The process 
of calcification of dentin (dentinification) which precedes that 



248 



DENTAL PATHOLOGY 



of enamel calcification (arnelification) by a few days advances 
from without inwards, the odontoblasts probably discharging the 
calcific material so as to envelop the protoplasmic process with 
which each odontoblast is provided at its external end. As cal- 
cification proceeds, a gradual recession of the odontoblasts oc- 
curs, and simultaneously with this there is an elongation of their 
external protoplasmic processes which, occupying the lumen of 
the tubes thus formed, become the dentinal fibers, or fibrillar, or 
fibers of Tomes. 

It is not at all improbable that the intertubular substance (den- 
tin matrix) is the result of the calcification of cells from the 



22 months aftvr birth 
18 months after hirth 



12 months after birth 



C months after birth 



40th week (birthl 
30th week embryo ' 
18th week embryo 
17th week embryo 




Fig. 115. — Calcification of the deciduous teeth. (Peirce.) 




4 years 
3 years 
2 years 
1 year 
At birth 



Fig. 116. — Calcification of the permanent teeth. (Peirce.) 

dental papilla, this process being likewise presided over by the 
odontoblasts. 



Cementum and Peridental Membrane 

As will be remembered, about the tenth week of embryonic life 
there are seen to grow out from the base of each dental papilla 
certain cells which become the fibrous envelope of the tooth germ 
(follicular wall) (Fig. 114). This closes simultaneously with the 
severance of the cord about the thirteenth week. This fibrous 
layer has a dual function: the cells of the outer layer are con- 



DEVELOPMENT OF THE TEETH 249 

cerned in the building up of the osseous structure of the alveolar 
process, those of the inner layer being concerned in the building 
of cementum. It should be added here, however, that a line of 
demarcation between the external and internal layer is prac- 
tically an impossibility. At the time of eruption of the teeth 
through the gums there still remain portions of the tooth root, 
cementum, and alveolar process to develop. The alveolar proc- 
ess is produced simultaneously with the cementum in order to 
provide for the means of retention of the tooth in the jaw. The 
process of root development is best studied from the diagrams 
(Figs. 115 and 116). 



CHAPTER XIII 

HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 

In the discussion of hypoplasia in its microscopic and macro- 
scopic aspects we aim to describe abnormalities of the teeth in 
structure, size, form and number. The term atrophy will not be 
used for the reason that in its general acceptance it conveys the 
thought of retrograde changes after an organ has attained its full 
growth, atrophy being denned as the series of changes taking 
place in a fully formed organ leading to a loss of weight, size 
and function consequent upon such causes as overuse, disuse, 
excessive pressure, faulty diet, and nutritional and trophic dis- 
turbances. Excess of waste over assimilation leads to atrophy. 

The teeth, barring pathologic conditions and the physiologic 
wearing away of their occlusal surfaces, remain unchanged 
throughout the life of the individual. They are not subject to 
retrogressive changes through overuse or lack of use, (exclud- 
ing, of course, the manifestations of these conditions upon the 
peridental membrane, which is not, strictly speaking, an integral 
part of the tooth, but accessory thereto), and neither are the hard 
tissues improved in quality, to much of an extent, 1 after they 
have become calcined. Enamel and dentin have no power of 
repair. We exclude from this consideration such calcifications 
as take place in the dentinal tubules as a normal process with 
advancing age, or as the result of pathologic influences. Also 
are excluded increases in the thickness of cementum of a strictly 
pathologic character, and the increases of cementum in certain 
areas, or the resorptions in others which take place continuously 
until such time as the entire complement of teeth has erupted 
and the occlusion for the given individual has become perma- 
nently established. All changes in the cementum, constructive 
or destructive in character, are governed, as will be studied later 
in the text, by either functional changes in the peridental mem- 
brane or by the influence of osteoclastic (cementoclastic) cells. 



1 See discussion of enamel on page 226. 

250 



HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 



251 



As the size, form, and structure — the latter up to certain limits — 
of the crowns of teeth appear after their eruption, so will they 
remain unaltered through life, except, of course, as the result of 
disease processes. 

DENTAL HYPOPLASIA 

Enamel, Dentin, and Cementum 

Imperfect or insufficient development of a part resulting from 
abnormal influences during intrauterine life, or during develop- 




Fig. 117. — Hypoplastic defects of the enamel. Incomplete calcification of the fissures 
and faulty development of the enamel rods in the area of a cusp, a, incomplete fusion 
of the cusps of a bicuspid resulting in a defecting calcified fissure; b, disturbance in the 
arrangement of the enamel rods. The histological characters of the enamel rods in the 
area at b, are wanting. 

mental periods after birth, is classified as hypoplasia. Under this 
heading the study of developmental defects of the enamel, den- 
tin, and cementum will be undertaken. 

Etiology. — By hypoplasia of the teeth is meant incomplete, de- 
fective or misdirected development of the tissues of the teeth. 
These developmental faults may be only microscopic, or both 



252 



DENTAL PATHOLOGY 



microscopic and macroscopic in character, and are dependent for 
their production upon unbalanced nutritional processes affect- 
ing the dental follicle at any time from the beginning of its for- 
mation to the completed development of the tooth, which is 
marked by the calcification of the apical portion of the root 




Fig. 118. — Hypoplastic defect of the enamel. Incomplete fusion of the cusps of 
molar producing a defective fissure as shown at c. Areas of normal enamel at a, a' 
a small area of normal dentin at b. 



and the establishment of the apical foramen as it will persist with 
whatever changes may occur in its diameter throughout the life 
of the tooth. The inorganic salts which enter into the formation 
of the enamel are not carried to the enamel organ in sufficient 
amounts as the result of faulty metabolism or of a diet poor in 
inorganic salts. Again, it may result from a defective combination 



HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 253 

between the inorganic salts and the albuminous binding sub- 
stance. 

The periods of nutritional insufficiency may be due to path- 
ologic conditions in the mother which will affect the deciduous 
teeth, directly, or in the advanced stages of development by hav- 
ing induced in the infant changes -affecting its physiological ac- 
tivities. It is well to remember in this connection that the be- 
ginning of calcification of these teeth is included in the period 
from the sixteenth to the twentieth week of intrauterine life. 
Disturbances in the mother interfering with the nutritional proc- 
esses in the fetus may. in some instances, affect the first per- 
manent molar, as the calcification of this tooth is known to begin 
in some cases one or two months before birth. The transmission 
from mother to fetus of certain systemic intoxications, particu- 
larly syphilis, may result in hypoplasia of certain teeth whose 
calcification does not begin until after birth. Concerning con- 
ditions after birth, it can be stated that any disease or deviation 
from the normal in the child may result in temporary arrests 
of calcification of the enamel and dentin, or in defective calci- 
fication; but particularly important are the exanthematous fevers 
— measles, chicken pox. scarlet fever, smallpox, etc. — which may 
leave a hypoplastic impression upon the enamel and dentin. A 
rise in temperature of whatever origin, if it persists for as little 
as a few days, may leave its permanent impress upon the teeth. 
Infectious processes in the roots of the deciduous teeth may cause 
changes in the underlying permanent tooth sac: resulting in de- 
fective calcification. 2 

Developmental defects of enamel affect certain areas of as 
many teeth as are in process of development at the time the nu- 
tritional errors were taking place. It is in this way that, knowing 
the chronology of tooth development, and in particular that of 
calcification of the enamel, it is a comparatively easy matter to 
ascertain the period in the life of the embryo or after birth 
when these disturbances of nutrition occurred. 

Histologically these defects in the enamel are due to insuffi- 
ciency in the number of enamel rods, imperfect calcification of 
the rods, and likewise to deviations in the quantity or quality or 



2 Turner. J. S.: Transactions Odontological Society of Great Britain, XXXVJT, in 
Bennett's Dental Surgery. 



254 



DENTAL PATHOLOGY 



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HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 



255 



both of the cementing substance (Figs. 117, 118, 119, and 120). 
Two interesting specimens of marked enamel hypoplasia are 
shown in Figs. 119 and 120. As previously stated, the histologic 
defect may be so intense as to give rise to a macroscopic defect 
visible on the external enamel surface, such being the case with 
the specimen under consideration. In Fig. 120 a disturbance in 
the disposition of the enamel rods has occurred. The rods, in- 
stead of following the perpendicular direction to the surface, as 




Fig. 119. — Hypoplasia of tlie enamel producing an external macroscopic defect on the 
labial surface of an incisor. At a is observed the area of disturbed enamel rod calci- 
fication; the enamel rods that are present are of a low grade of calcification and stunted 
in their growth and the interprismatic substance is not present in sufficient amounts. 
Normal enamel is seen at b and b' : normal dentin at c and c' , and defects in the calci- 
fication of the dentin in the form of interglobular spaces at d. 



is the case in approximal surfaces, appear wavy and very irregu- 
lar in their course and faulty in their calcification. The more 
marked cases show a deficiency or absence of enamel, and the 
surface of the tooth is irregular and rough. 3 (Fig. 119.) 

Cases of complete or partial absence of enamel are also occa- 
sionally encountered. This form of exaggerated enamel hypo- 



3 Bennett: Dental Surgery, New York, Wm. Wood & Co. 



256 



DENTAL PATHOLOGY 



plasia is designated under the term of enamel agenesia (Fig. 
121). Systemic disturbances of a severe type undoubtedly occur 
at the calcification period of the affected teeth. 

In the dentin, hypoplastic defects are represented by imperfect 
tubular formation, incomplete tubular calcification, and defects in 
the dentin matrix (Fig. 122). 

These hypoplastic changes are manifested in the shape of an 
increase in the size and number of the interglobular spaces. These 



.&*■; . 


: ,V- 


* \ . •■ . * I '"• ■ 



Fig. 120. — Hypoplasia of the enamel in the approximal surface of an incisor. At 
a, a' enamel rods which do not follow the direction of normal enamel rods in these loca- 
tions are seen. Also the abrupt decrease in the thickness of the enamel, from left to 
right of the picture should be observed. 



spaces are found in the dentin throughout the entire extent of the 
tooth, but are more prominent near the enamel. They represent 
stages of arrested activity of the odontoblastic layer. Any patho- 
logic influence strong enough to produce hypoplasia of the enamel 
will likewise produce arrested calcification in certain areas of the 
dentin. The formation of tubules will come to a standstill, and 
upon the recovery of the formative organ the formation of tubules 
will begin at some distance from the point where growth had 
stopped. The sections of organic matrix which undergo partial 



HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 



257 




Fig. 121. — A case of enamel agenesia. All the deciduous teeth are affected. The 
dentin is nowhere protected by enamel and is of a yellowish color typical of dentin when 
exposed to the fluids of the mouth and to extraneous substances. 





Fig. 122. — Decalcified section showing a multitude of interglobular spaces. These 
are areas of incomplete development and calcification of the dentin matrix and dentinal 
tubuli. a, cementum (hyaline); b, normal dentin; c,d,e,f, interglobular spaces of 
Czermak. 



258 DENTAL PATHOLOGY 

calcification, or do not undergo any calcification at all, constitute 
the interglobular spaces first described by Czermak after whom 
they are named the inter globular spaces of Czermak. 

Examples of hypoplasia of the deciduous teeth are rare: when 
it occurs it is located high in the crowns toward the gingival mar- 
gin, the occlusal surfaces being almost invariably normal. The 
reason for this lies in the fact that the period of greatest suscepti- 
bility to abnormal influences in utero, so far as the teeth are con- 
cerned, is during the last month or two of intrauterine life, and 
reaches to the beginning of the second year after birth. On the 
other hand, hypoplasia of the permanent teeth is relatively frequent 
in some teeth, while others are rarely affected; e.g., the bicuspids 
and second molars are seldom the seat of hypoplasia, while the third 
molars upper and lower are frequently the seat of defective 
development affecting the crown or roots of the tooth, or both, and 
is in practically all instances the result of obstructions in the path 
of their eruption. 

Pathologic Anatomy. — In the study of structural hypoplasia of 
the enamel or dentin any deviation from the appearance of mi- 
croscopic sections which are within the limits of normality is to 
be considered as a developmental (hypoplastic) defect. By this 
we mean that the enamel should have a uniform appearance, and 
the rods under high magnification should show the transverse 
markings indicative of the method of individual rod formation 
(Figs. 88 and 89). In the case of the enamel, the lack of cement- 
ing substance produces the white spots so frequently encoun- 
tered, also spots from the faintest to the deepest shade of brown. 
Two cases of extensive enamel hypoplasia are reported by the 
late Dr. G. V. Black 4 in which a general absence of cementing 
substance was responsible for an enamel Avhich was white, chalky, 
and easily disintegrated. In these places the enamel is so easily 
disturbed or penetrated by means of a cutting instrument that an 
explorer, after the surface has been penetrated, will in some ex- 
aggerated cases convey a sense of chalkiness. These white spots 
may or may not affect the entire thickness of enamel. Patho- 
logically these are significant defects because of their offering 
favorable areas for the rapid spread of caries. Imperfect enamel 
calcification is frequently encountered in the fissures of molars and 



4 Black, G. V.: Operative Dentistry, i. 






HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 



259 




Fig. 123. 



Fig. 124. 



Fig. 123. — Hypoplasia of the Fig. 124. — Hypoplasia of the enamel in the shape 

enamel in the shape of a slight of intense reddish brown discoloration, 
reddish brown discoloration. 




Fig. 125. — A case of brown stain affecting the enamel on the labial surfaces of the central 
and lateral incisors only. 



bicuspids, and in the lingual pit of the upper central and lateral 
incisors, when the pit is present; in the linguogingival ridge of 
the upper cuspid, when fissured or grooved ; in the buccal groove 
of the upper first molar. In these locations the defect is due 
to incomplete closure of the fissure. 



260 



DENTAL PATHOLOGY 





Fig. 126. — A slight hypoplasia of the Fi| 

enamel on the. labial surface of an upper the 1; 
cuspid. 



127. — Hypoplasia of the enamel on 
al surface of an upper cuspid. 




Fig. 128. —Hypoplasia of the enamel on the Fig. 129. — Hypoplasia of the enamel 

labial surfaces of upper left and upper right in an upper left central incisor. The 
lateral incisors, semilunar in shape. enamel is transversed by horizontal 

and vertical depressions of a brown 

color. 



The formation of rods has been insufficient to produce a smooth 
bridging over or closure of the fissure. A large number of sec- 
tions which have been examined in the course of our studies show 
frequently the presence of calcified amorphous bodies in these 
defective fissures. In the milder forms of hypoplasia the bands 



HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 



261 



of Retzius appear larger and are of a deeper brown color than is 
the case in normal specimens, testifying to a lack of uniform cal- 
cification of the rods in their long diameter. The enamel beinsr 





Fig. 130. — Hypoplasia of the enamel in 

an upper right lateral incisor. 



; !. ll>! oplasia in the crown of a 
lower molar. The enamel is studded 
everywhere with soft chalky spots (chalky 
enamel). 




Fig. 132. — Hypoplasia 
of the crown of an upper 
molar. The enamel, as in 
the previous picture, con- 
tains a large number of 
chalky areas. 



Fig. 133. — Hypoplasia of the enamel in upper molars. The 
extent of the faulty development is shown externally by an 
extreme irregularity of surface upon the occlusal and approx- 
imal aspects of the teeth. 



deposited in segments represented by the bands of Retzius, it 
stands to reason that any disturbance which will affect the proc- 
ess of enamel formation will be represented by variations from 



262 



DENTAL PATHOLOGY 



the normal throughout the segment of enamel in the course of 
deposition. Inasmuch as insufficient or imperfect enamel forma- 
tion is the result of a temporary arrest of activity throughout 
the extent of the ameloblastic layer, it consequently follows that 
all enamel that would have been formed, in the absence of disturb- 




Fig. 134. — Hypoplasia of the enamel in lower molars. The occlusal and approximal sur- 
faces, as in previous specimen are extremely irregular. 




Fig. 135. — Hypoplasia of tlie enamel in 
an upper cuspid. Several faint lines run- 
ning horizontally across the enamel mar 
the appearance of the crown. 




Fig. 136. — Hypoplasia of the enamel in 
an upper central. The band in the cen- 
ter of the crown is the dividing line be- 
tween two periods of hypoplasia which oc- 
curred at different times. The incisal 
third, the gingival third, and the "band" 
are the normal enamel areas of the tooth. 



ing factors, is affected. While this view is upheld by a number of 
pathologic investigators, instances have come under our own ob- 
servation in which the defective formation has not followed a 
segment or band of Retzius in its entirety, but has manifested it- 



HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 263 

self in the shape of a relative preponderance of cementing sub- 
stance throughout the depth of several segments in the direction 
of the enamel rods. The greater amount of cementing substance 
at the sacrifice of the number of enamel rods is characterized 
microscopically by dark, cloudy areas surrounded by enamel rods 
of normal appearance. This increase in the depth of color is be- 
lieved to be due to the presence of actual pigment. 5 

Developmental defects in the enamel and dentin, when pro- 
nounced, give rise to conspicuous malformations of the crown 
which may range from the slightest brownish discoloration, as 
seen in Fig. 123, to most marked brown spots in the enamel as 
seen in Figs. 124 and 125, and from the faintest chalky whiteness 
in the enamel, as seen in Fig. 126, to as pronounced a hypoplasia as 
seen in Figs. 127 to 134. Again, from a faint line or lines in the 
enamel (Fig. 135) sufficiently pronounced to mar its appearance to 
as wide a band as that shown in Fig. 136. In other cases several 
grooves may be present in the labial side of the crown, and in still 
others the hypoplastic defects assume a rough granular or pitted 
appearance — the granular defect of the enamel. 

The pit form of enamel defect consists of either one single pit 
surrounded by healthy enamel structure, or of a series of pits ; 
the former may be located anywhere on the enamel surface, the 
latter in the lower half of the crown near the incisal edge in the 
case of the incisors or cuspids or near the occlusal surface in the 
case of the bicuspids or molars. The more pronounced develop- 
mental defects will be discussed under the heading of macroscopic 
deformities of the teeth in the following chapter. 



5 Noyes : Dental Histology and Embryology, Philadelphia, Lea & Febiger. 



CHAPTER XIV 

MACROSCOPIC DEFORMITIES OF THE TEETH 

Macroscopic deviations from the normal may affect the crown, 
the root, and both the crown and the root of one tooth, of several 
teeth, or of all the teeth in the same mouth. These macroscopic 
deviations may be so slight as to require careful examination in 
order to detect them. In these cases the external appearance of 
the tooth is slightly affected and the physiologic function not at 
all. In other instances the deviation from the normal is so ex- 
tensive as to mar the appearance of the tooth to the point of ren- 
dering its identification difficult and its physiologic function incom- 
plete. Gross deviations in size ma}' affect one or more teeth, or all 
of the teeth in both arches. It is not unusual to find that one tooth 
is larger or smaller in relation to the other units of the same arch, 
and again that all the teeth in both arches are either too small or too 
large in relation to the size of the mouth and to facial contour. 
The upper central incisors and canines, the lower second bicuspid 
and the third molars, upper and lower, are frequently out of 
harmony with their fellows in the arch. Other types of abnor- 
malities in size consist in a disproportion in the size of the crown 
and root, as is seen in the case of central incisors with abnor- 
mally short roots and upper cuspids with abnormally long or 
short roots. Under a different heading will be studied those ab- 
normalities affecting the number, of teeth in the arch, i.e., the 
presence of supernumerary teeth, and the congenital absence of 
one or more units from the dental arch. 

Abnormalities of Form Affecting the Crowns and Roots of the 

Permanent Teeth 

Central Incisors. — The most important macroscopic defects in 
the central incisors are those which affect the cervicolingual 
ridge. This ridge may be either insufficiently developed or over- 
developed to such an extent as to result in the presence of a pseudo- 
cusp (Figs. 137 and 138). The division of the cervicolingual ridge 

264 



MACROSCOPIC DEFORMITIES OF THE TEETH 



265 



by a nearly central fissure, as seen in some instances, results in the 
presence of two cervicolingual ridges — a mesiolingual and a disto- 
lingual ridge. 1 (Fig. 139.) In Fig. 140 a reproduction of a 





Fig. 137. — Overdeveloped cervicolingual Fig. 139. — Fissured cervicolingual ridge 

ridge in upper left lateral incisor. in lateral incisor. 




Fig. 138. 



ypoplasia of the cervicolingual ridge of upper incisors. 



ground section of an incisor with an overdeveloped cervicolingual 
ridge simulating a cusp, is seen. An extra root arising from the 
lingual aspect is another abnormality that may affect this tooth. 



Bennett: Dental Surgery, New York, Win. Wood & Co. 



266 



DENTAL PATHOLOGY 



A disproportion between the size of a crown and its root may 
exist. The central incisors may be the seat of severe hypoplasia. 
(Figs. 141, 142, and 143.) The root only may be imperfectly 
developed (Fig. 144). A ground section shows normal microscopic 
characteristics, notwithstanding the macroscopic root deformity 




Fig. 140. — Photomicrograph of a central incisor with an overdeveloped cervicolingual 
ridge simulating a cusp, a, dentin; b, enamel; c, hypoplastic defect of the enamel in the 
under surface of the cervicolingual ridge. 



(Fig. 145). A hypoplastic defect of the middle lobe of the central 
incisor, the so-called Hutchinson's notch, is shown in Fig. 146. 

The upper central incisors are in some instances much larger 
in size in proportion to their neighbors. When present, this ab- 



MACROSCOPIC DEFORMITIES OF THE TEETH 267 

normality in size generally affects both, 2 the right and left cen- 
tral incisors. 

Upper central incisors with abnormally short roots are some- 
times encountered. 





Fig. 141. — Severe hypoplasia of upper ; 42. — Severe form of hypoplasia in 

central incisor, embodying the microscopic upper incisor, embodying the microscopic 

and macroscopic forms. and macroscopic forms. 





Fig. 143. — Severe form of hypoplasia in Fig. 144. — Hypoplasia of the root of an 

upper incisor involving the crown and upper incisor, 
the root. 

The lower central incisors are rarely the seat of abnormalities. 
Lateral Incisors. — The upper lateral incisors may be the seat 



-Burchard and Inglis: Dental Pathology and Therapeutics, Philadelphia, Lea & 
Febiger. 



268 



DENTAL PATHOLOGY 



of macroscopic defects of the same character as found in the 
central incisors, i. e., underdevelopment or overdevelopment of 
the cervicolingual ridge and the presence of an additional root. 
The lower lateral incisors are rarely the seat of abnormalities. 
The upper lateral incisor is frequently the seat of marked macro- 
scopic aberrations, the crown assuming various shapes, in addi- 




Fig. 145. — Ground section of specimen shown in Fig. 144. It shows normal microscopic 
characteristics, notwithstanding the gross root deformity. 



tion to a disproportion between the size of the crown and that 
of the root, A peg-shaped lateral is occasionally encountered 
(Fig. 147). The root of the upper lateral incisor may be de- 
flected labially, as seen in Fig. 148. Upper lateral incisors are 
sometimes found with abnormally deep cervicolingual ridges and 
a median fissure two-thirds across their vertical diameters. A 



MACROSCOPIC DEFORMITIES OF THE TEETH 



269 



lower lateral incisor with a prong-like process on the lingual 
surface is seen in Fig. 149. 

The lower lateral mav have two roots and two root canals (Fi^ 
150). The two roots may be well formed and independent of one 





Fig. 146. — Hypoplasia of the incisal 

third of an u 



Fig. 147. — Peg-shaped upper lateral 



rig. i-hj. — n\popias.ia ui wie inumi rig. i-f/. — reg-snapeu upper lateral in - 

third of an upper incisor. A so-called cisor. As the length of the picture is 

Hutchinson's tooth. The middle lobe is twice the actual length of the tooth it does 

incompletely developed upon the incisal not convey a clear idea of the diminu- 

aspect. tiveness of the tooth. 





Fig. 14S. — An upper right lateral in- 
cisor mesial view with a labial deflec- 
tion of its root. 



Fisr. 149 — A prong-like process on the lin- 
gual surface of the lower lateral incisor at a. 



another, or the deformity may consist of the bifurcation of its 
normal root at the apical third. 

Cuspids. — With the exception of a disproportion in the size 
of this tooth as compared with the other teeth in the same arch, 
the cuspid is rarely the seat of macroscopic defects, although 



270 DENTAL PATHOLOGY 

overdevelopment of the cervicolingual ridge may be encountered, 
and in some instances it is so marked as to simulate a lingual 
cusp. Two cases of severe hypoplasia of the crown of an upper 
cuspid are seen in Figs. 151 and 152. 

A series of short-rooted upper cuspids is shown in Fig. 153. A 
series of long-rooted upper cuspids is shown in Fig. 154. The 
deflection, if there is any, of the root of the upper cuspid is as a 






Fig. 150. Fig. 151. Fig. 152. 

Fig. 150. — Lower lateral incisor with two roots. 

Fig. 151. — Severe hypoplasia of upper cuspid. (Microscopic and macroscopic defects.) 

Fig. 152.. — A marked case of enamel and dentin hypoplasia (microscopic and macro- 
scopic defects) in upper right cuspid the result of an exanthematous fever from which 
the patient suffered at the time at which the tooth was being calcified. The defect and 
incomplete development has affected both the enamel and dentin. 

general rule in a distal direction (Fig. 155), but it may be in a 
mesial direction, as shown in Fig. 156. 

The occurrence of two-rooted lower cuspids is not rare. Speci- 
mens of this type of malformation are shown in Figs. 157 and 
158. The lower cuspid may have an abnormally short root. A 
supernumerary root in a lower cuspid occasionally occurs (Fig. 
159). A severe hypoplasia of a lower cuspid is seen in Fig. 160. 



MACROSCOPIC DEFORMITIES OF THE TEETH 



271 



Bicuspids. — The upper first bicuspid may have a crown with 
three cusps and a trifurcated root as shown in Figs. 161 and 162 ; 
also, instead of the usual bifurcated root it may have a single root 
with two canals and two apical foramina, or one root with one sin- 
gle canal constricted mesiodistally. In the upper second bicuspid, 
when the root is bifurcated, the two branches may be united by a 




Fig. 153. — A series of upper cuspids with unusually short roots. 




Fig. 154. 



of upper cuspids with abnormally long roots. 



band of cementum for some distance from the bifurcation to the 
apices of the roots, as shown in Fig. 163. The lingual root of the 
upper first bicuspid may be deflected to the extent shown in Fig. 
164. The root of the upper second bicuspid may be abnormally 
small and stubby, dividing into two branches in the apical region, 
as shown in Fig. 165. In the case of three-rooted upper bicuspids 



272 



DENTAL PATHOLOGY 





Fig. 155.— Distal deflection of 
per right cuspid. 



Fig 

mesial 



156. — A marked deflection to the 
n an upper right cuspid. 




Fig. 157. — Lower cuspids with two roots. 



MACROSCOPIC DEFORMITIES OF THE TEETH 



273 




Fig. 158. — Radiogram of a lower right cuspid with two roots. 




Fig. 159. — Supernumer- 
try root in lower cuspid. 





Fig. 160.— Marked hy- 
poplasia of the crown of a 
lower cuspid. 



Fig. 161. — Upper first 
bicuspid with three roots. 




Fig. 162. — Upper right 
first bicuspid with three 
roots. 



Fig. 163. — An upper 
second bicuspid with a bi- 
furcated root. 



Fig. 164. — An upper 

first bicuspid with marked 

deflection of the lingual 
root. 



274 DENTAL PATHOLOGY 

the disposition of the roots may assume either one of two relation- 
ships: (a) there may be present a mesiobuccal, a distobuccal and 
a lingual root (Fig. 161) ; or (b) one root may be on the buccal as- 
pect and the other two on the lingual aspect of the tooth, as shown 
in Fig. 166. There may exist a disproportion between the crown 
of the upper first bicuspid and its root, as shown in Fig. 167. A 





Fig. 165. — Bifurcation of the roots of Fig. 166. — An upper bicuspid with 

an upper second bicuspid. three roots ; one root is placed buccally and 

two lingually. 






Fig. 167.— An upper Fig. 168.— A hypoplas- Fig. 169.— Pronounced 

first bicuspid with an ab- tic upper bicuspid. deflection of the root of an 

normally long root. upper bicuspid. 

hypoplastic upper bicuspid, probably the first, is seen in Fig. 168, 
and in Fig. 169 a view of an upper bicuspid with a marked deflec- 
tion of the root. 

The upper second bicuspid may present variations affecting the 
number and size of its roots. As a general rule this tooth has but 
one root and one canal, the latter having its longest diameter in a 
buccolingual direction. Deviation from this type may consist in 



MACROSCOPIC DEFORMITIES OF THE TEETH 



275 






Fig. 170.— Upper left 
second bicuspid; dispropor- 
tion between the size of the 
crown and that of the root. 



Fig. 171. — An upper Fig. 172. — A lower 

second bicuspid with a first bicuspid with two 

disproportionately small roots, 
root. 





Fig. 173. — Lower sec- 
ond bicuspid with two 
roots. The lingual root 
is partly hidden behind 
the buccal. 



Fig. 174. — A lower first 
bicuspid with a marked de- 
flection of its roots. 



Fig. 175.— Distal deflec- 
tion of the root of the 
lower right first bicuspid. 



276 



DENTAL PATHOLOGY 





Fig. 176. — Disproportion between the 
size of the crowns and mots of lower 
second bicuspids. Also deflection of the 
roots rendering practically impossible the 
proper treatment and tilling of the root 
canal. 



Fig. 177. 



-Hooked root in lower 
bicuspid. 








Fig. 178.— Disproportion between 

the crown and root of a lower right 
second bicuspid. 



Fig. 179. — Disproportion between the size 
of the crown and that of the root and deflec- 
tions of the root of lower first bicuspids. 



MACROSCOPIC DEFORMITIES OF THE TEETH 



277 



the presence of two or three roots, each with its respective root ca- 
nal. Disproportion between the size of the crown and that of the 
root of the upper second bicuspid is seen in Figs. 170 and 171. 

The lower first bicuspid may have a lingual cusp larger or 
smaller than the average type of lingual cusp for this tooth. The 





Fig. 180. — Hypoplasia of the lingual 
cusp of a lower first bicuspid. 



Fig. 181. — A hypoplastic lower second 
licuspid. 





Fig. 182. — Lower left second bicuspid with six cusps. Lingual and occlusal views. 
simulating an abnormal lower third. A, buccal aspect; B, occlusal aspect. 

lingual cusp of the lower first bicuspid is even in normal speci- 
mens markedly smaller than the buccal cusp, but in some abnormal 
specimens it is nothing more than a rudimentary cusp. The lin- 
gual surface of the crown may be free from fissures, or the lin- 
gual cusp may be bordered on the mesial and distal by a fissure 
which, beginning near the mesial and distal marginal ridges, 
reaches over onto the lingual surface. Also, first and second lower 



278 



DENTAL PATHOLOGY 



bicuspids with two roots and two distinct root canals are occasion- 
ally found. A lower first bicuspid with two roots is a rare ab- 
normality (Fig. 172). A lower right second bicuspid with two 





Fig. 183. — The roots of an upper molar Fig. 184. — An upper second molar with 

united by bands of cementum. its three roots fused together by means 

of cementum. 





Fig. 185. — Upper left third molar with Fig. 186. — An upper first molar with 

badly deflected, fused and hypercemen- hooked roots, 
tosed roots. 



roots is seen in Fig. 173. In these cases the roots may be fused for 
a section of their length by means of a band of cementum or 
throughout the length of the roots. A marked deflection of the 



MACROSCOPIC DEFORMITIES OF THE TEETH 



279 



root of the lower first bicuspid is sometimes found, as shown in 
Fig. 174. The deflection in this case was toward the lingual. A 
distal deflection of the root of the lower first bicuspid is seen in 
Fig. 175. A disproportion between the size of the crown and that 
of the root of the lower second bicuspid, and a deflection of the 
root is seen in Fig. 176. A hooked root in a lower bicuspid ren- 
dering impossible successful root canal treatment and filling is 
shown in Fig. 177. 

Disproportion between the size of the crown and that of the root 
is not an infrequent occurrence in the case of the lower bicuspids. 
The root is proportionately either considerably longer or shorter 





Fig. 187. — Deflection to buccal and dis- 
tal roots of upper first molar. 



Fig. 188.— A 
upper molar. 



supernumerary root in 



Than the crown, or vice versa (Figs. 178 and 179). The dispropor- 
tionately long root may be either deflected, or hypercementosed, or 
both. These root deflections and the fact that the abnormally long 
root not infrequently has a very slender termination, render dim- 
cult, if not impossible, the treatment and filling of the root canal. 
Hypercementosis of the abnormally long root of a lower first bi- 
cuspid is not an uncommon phenomenon. 

The lower second bicuspid may present a disproportion between 
the crown and the root. The root may be either too short or too 
long. The root may be extremely deflected, usually to the left. 
Figs. 180, 181, and 182 are reproductions of hypoplastic lower 
bicuspids. 



280 



DENTAL PATHOLOGY 



First Molars. — A not infrequent macroscopic abnormality in 
the upper first molars is the presence of a cusp between the mesial 
and lingual cusps in the gingival margin. An elevation in some 





Fig. 189. — Lower right first molar with 
supernumerary root on the lingual aspect. 



Fig. 190. — Supernumerary root on disto- 
huccal aspect of a lower first molar. 




Fig. 191.— A lower first 
molar with a supernumer- 
ary root between the me- 
sial and distal roots on the 
lingual aspect. 



Fig. 192. — A lower 
first molar with three 
roots. The supernumer- 
ary springs from the dis- 
tal root. 



Fig. 193.— A lower first 
molar with three roots; su- 
pernumerary root on inci- 
sal aspect. 



portion of the occlusal surface simulating an additional cusp is 
another form of abnormality found in this tooth. The roots of the 
first molar are generally well developed and independent of one 
another. There is, however, in some cases, a fusion of the two 






MACROSCOPIC DEFORMITIES OF THE TEETH 



281 



buccal roots, or of one buccal root with the lingual root, or of 
the three roots, the latter being a rare occurrence. These fusions 
are due to a growth of cementum between the roots (Figs. 183, 
184, and 185). The roots of the upper first and second molars 
may be markedly deflected and hooked (Figs. 186 and 187). A 
diminutive supernumerary root may be present on an upper molar 
(Fig. 188). 

The lower first molar is sometimes minus the distal buccal cusp. 
Tomes found this cusp absent in 18 per cent of a series of skulls 
examined by him. 4 

The abnormalities of this tooth consist in the presence of a super- 





Fig. 194. — Four well-developed roots 
in lower left second molar. 



Fig. 195. — A hypoplastic lower third 
molar. 



numerary root in relation with the distal root (Fig. 189). This 
extra root is usually located on the lingual aspect of the tooth, 
but may be also found on the buccal aspect of the tooth (Fig. 
190). In Fig. 191 is seen a lower first molar with an extra root be- 
tween the mesial and distal roots on the lingual aspect. A lower 
first molar with a bifurcated distal root is seen in Fig. 192. A 
lower first molar with a supernumerary root in relation to the 
mesial root is seen in Fig. 193. 

Second Molars. — The upper second molar may be a three- in- 
stead of a four-cusped tooth, in which case the crown is of a 



4 Bennett: Loc cit 



282 



DENTAL PATHOLOGY 



quasitriangular shape, and the roots are completely fused by 
means of cementum. The three roots of this tooth are frequently 
subject to abnormal variations. The lower second molar is, how- 




Fig. 196. — Dwarfed upper third molar. 




Fig. 197. — Dwarfed lower third molai 




Fig. 198.- — Dwarfed upper third molar. 



ever, less frequently the seat of abnormal development than the 
first molar. The roots may converge at their apices. 5 A lower 
second molar may present four well-developed roots (Fig. 194). 



Barrett: Loc. cit. 



MACROSCOPIC DEFORMITIES OF THE TEETH 



283 



Third Molars. — The third molar is frequently the seat of ab- 
normal development. From the almost perfect upper and lower 
third molars closely resembling their respective second molars, 
every type of deviation is found, even down to the dwarfed molar. 





Fig. 199. — Hypoplastic upper third 
molars. 



Fig. 200.— Marked deviation of the 
roots of an upper third molar. 




Fig. 201. — Upper third molars with double deflection of the buccal roots and single de- 
flection of the lingual roots. 

The lower third molar may present a fairly well-developed crown 
having three short roots fused together, as shown in Fig. 195. It may 
also present a supernumerary root located between the mesial 
and the distal roots. The upper and lower third molars may be 



284 DENTAL PATHOLOGY 

as insufficiently developed as shown in Figs. 196, 197, and 198. In 
Figs. 199 and 200 are shown upper third molars with marked 
developmental deviations. An upper third molar with double 
deflection of the buccal roots is shown at Fig. 201. 

The upper third molars may exhibit roots so badly curved as to 
render any attempt at root canal treatment absolutely impossible. 
A supernumerary root may be present, springing from the base 
of the lingual root. 

Lower third molars are, as a rule, possessed of roots which are 
deflected distally to various extents. The mesial and distal roots 
may be single deflected cones, terminating in a very slender tip, 
or the distal root may be a single deflected cone and the mesial 
root bifurcated — an incomplete fusion of the mesiobuccal and 
mesiolingual roots. The mesial and distal roots may be fused 
into one single cone in which the lines of fusion make it possible 
to segregate them. The fusion in such cases may be complete or 
only partial, a space being present between the bifurcation and 
the beginning of fusion. When the two roots are fused, the 
joined apices may or may not be deflected to the distal. Oc- 
casionally a lower third molar is encountered with two roots 
which, bifurcating near the apex, give the tooth the appearance 
of having four roots. The mesial root, whether bifurcated or 
not, may be proportionately much shorter than the distal root. 
A rootlet may occasionally be found between the two roots upon 
their lingual aspect. 

Geminated Teeth 

By geminated teeth is meant the fusion of two or more teeth 
by means of enamel or cementum. During the developmental 
period it is probable that distortion by pressure of the enamel 
organs of the fused teeth takes place, and again, this distortion 
or misplacement may affect the developing roots only, in which 
case the crowns will be separated from one another, but the 
roots will be fused or united by means of cementum. The fusion 
or gemination of teeth may affect either the deciduous or the 
permanent teeth. Fig. 202 shows two deciduous incisors erupted 
with their roots fused to one another by means of cementum. Fig. 



MACROSCOPIC DEFORMITIES OF THE TEETH 



285 



203 shows an upper central and lateral incisor erupted fused to 
one another for a distance of about one-third the length of their 
roots from their apices to an imaginary line of junction between 
the apical third and gingival two -thirds. In Fig. 204 a molar 





Fig. 202.— Geminated 
deciduous incisors. 



Fig. 203. — Geminated up- 
per central and lateral inci- 
sors. 





Fig. 204. — Geminated molar and 
bicuspid; possibly two bicuspids. 



Fig. 205. — Geminated upper second 
and third molars. 



and bicuspid, possibly two bicuspids, are shown, the crowns and 
one half of the roots being fused together. In Figs. 205, 206, 
and 207 upper second and third molars are shown fused to one 
another in their roots. 
Distortions and displacements of portions of the enamel organ 



286 



DENTAL PATHOLOGY 



result occasionally in the presence of enamel tissue in abnormal 
locations. In Fig. 208 is seen a rounded mass of enamel tissue 
(enamel pearl) in a concavity on the lingual root of an upper 




Fig. 206. — Geminated upper 
second and third molars. 



Fig. 207. — Geminated upper second and third 

molars. 




Fig. 208. — Enamel pearl on upper 
left second molar located in the 
concavity on the lingual root which 
shows a tendency toward bifurca- 
tion. 




Fig. 209. — Enamel pearl in upper 
right first molar. 



left second molar, and in Fig. 209 is seen an enamel pearl in an 
upper right molar at the neck of the tooth. 



CHAPTER XV 
ABNORMALITIES IN THE NUMBER OF TEETH 

Supernumerary Teeth 

Abnormalities of number in excess, i. e., supernumerary teeth, 
are encountered more frequently than abnormalities due to the 
absence of teeth. A supernumerary tooth may be of abnormal 




Fig. 210. — A peg-shaped supernumerary tooth between the upper central incisors. 




Fig. 211. — Two tuberculated supernumerary incisors in the same arch. 

form or may have a normal appearance, usually that of one of 
its immediate neighbors. A supernumerary peg-shaped tooth is 

287 



288 



DENTAL PATHOLOGY 




Fig. 212. — A tuberculated supernumerary tooth between the incisors. The left central 
incisor is not shown in this view as it was located lingually. 




Fig. 213. — A peg-shaped supernumerary tooth located lingually to the upper incisors. 




Fig. 214. — A supernumerary central in perfect alignment between normal incisors. 



SUPERNUMERARY TEETH 



289 



at times found between the two central incisors, causing a very un- 
sightly malformation (Fig. 210). One or two supernumerary tu- 
bercidated incisors may be present in the same arch (Figs. 211 and 




Fig. 215. — A supernumerary upper incisor fused to the normal central incisor. 




Fig. 216. — Supernumerary molar between the upper second and third molars. 




Fig. 217. — A fourth molar in ph 



212). A peg-shaped supernumerary tooth may be located imme- 
diately behind one of the normal incisors, the latter being forced out 
of normal alignment (Fig. 213). The supernumerary incisor may 



290 DENTAL PATHOLOGY 

also be of normal form; Fig. 214 shows a case in which five in- 
cisors were present, each tooth having attained practically normal 
development. A supernumerary upper right lateral incisor of 
normal form may be located lingually from the central incisors. 
A supernumerary incisor may erupt fused to either one of the 
normal incisors (Fig. 215). In the molar region a reversion of 
type, as exemplified by the presence of a fourth molar on both 
sides of each arch, is not infrequently observed. The supernu- 
merary molar may be smaller in relation to its fellows, but still of 
somewhat regular form (Fig. 216). In Fig. 217 is shown a super- 
numerary molar (fourth molar) occupying a position distal to 
the third molar. A unicuspid tooth is sometimes found occupy- 
ing a position between the first and second molars on the buccal 
side. 



CHAPTER XVI 
ABNORMALITIES IN THE NUMBER OF TEETH 

Absence of Teeth 

Etiology. — The absence of teeth from the arch may be due to 
the noneruption of fully calcified teeth; to nonevolution of the 
tooth germ; to the failure of calcification processes in the dental 
follicle ; to injury to the developing tooth germ from traumatism or 
infectious processes; to the accidental removal of the permanent 
tooth germ by the extraction of the deciduous tooth ; to the trans- 
formation of the tooth germ into an odontoma. 1 

Whenever a calcified tooth does not erupt, il is a ease of in- 
carceration or impaction according as to whether the path lead- 
ing to normal position in the arch is free or obstructed. This ab- 
normality affects the third molars, upper and lower, the upper 
second bicuspids, the upper laterals and upper and lower cuspids 
with greater frequency than other teeth. Incarceration of a 
permanent tooth is sometimes associated with the retention of 
the corresponding deciduous tooth until later in life than normal. 
and occasionally even throughout the life of the individual (Figs. 
218 and 219). The influence of heredity in these abnormalities 
of number is well shown in the case of the upper laterals, this 
tooth being sometimes absent through several generations, in one 
or several members of the same family. 

R. M. Capon 2 has reported on the mouths of a whole family, 
parents and seven children, the youngest twelve years of age 
and the eldest twenty-seven, from which no less than twenty- 
seven of the permanent teeth missing had never erupted. The 
mouths of the three girls showed a deficiency of eight teeth. The 
eldest of the three had never erupted the upper lateral incisors 
and two of the lower bicuspids. The other two girls have some 
of the bicuspid teeth missing. One of the girls at the age of 



'P.ennett: Dental Surgery. 
-Capon, R. M.: Dental Record. 



291 



292 



DENTAL PATHOLOGY 



sixteen retained the temporary laterals. The boys, four in num- 
ber, have between them a deficiency of eighteen teeth. The father 
had never erupted the upper lateral incisor, and the mother is 
the only member of the family in whom all the teeth have 
erupted. 

While the absence of the complete dentition, both deciduous 
and permanent, and of the permanent alone, is an extremely rare 
occurrence, nevertheless cases of this kind are on record in den- 
tal literature. Bennett reports a case in which the upper cuspids 
occupjdng positions near the median line, one upper molar on 
each side, and one lower molar, also on each side, were the only 
teeth of the permanent set to erupt. An insufficiency in the num- 
ber of teeth is less frequently encountered than an excess (super- 





Fig. 218. — Deciduous upper second mo- Fig. 219. — A retained lower left second 

lar retained until late in life, occupying deciduous molar. The tooth follicle of the 

the position of the upper second bicuspid second bicuspid evidently never developed, 
which never developed. 



numerary teeth). In one extreme case the deciduous upper cen- 
tral and lateral incisors on the left side, and the deciduous 
central incisor on the right side, had been shed, and up to the 
age of nine years there was no indication that their permanent 
successors would erupt, the space between the right lateral in- 
cisor and left cuspid being occupied by one peg-shaped tooth. 

The absence of the permanent upper right lateral incisor is a 
rather frequent abnormality. A case of this kind is shown in 
Fig. 220. The absence of a lower incisor is a rare abnormality. 
A lower bicuspid may be absent and when it fails to erupt it is 
the second more frequently than the first (Fig. 219). The per- 
manent first molar may be absent owing to the failure of the fully 



ABNORMALITIES IN THE NUMBER OF TEETH 



293 



calcified tooth to erupt, its presence in the substance of the jaw 
being made evident with the aid of radiography. A case of this 
kind which gave rise to systemic complications, is shown in Fig. 
221. The absence of the permanent cuspids is rarely the result 




Fig. 220. — Absence of the upper right lateral incisor. 




Fig. 221. — Noneruption of permanent lower first molar. 



294 



DENTAL PATHOLOGY 



of the nondevelopment of the tooth, but in most instances is due 
to the failure of the fully formed tooth to erupt (Figs. 222 and 
223). The absence of deciduous teeth is occasionally ob- 
served. In extreme cases perhaps only the deciduous cuspids 
and second molars will erupt. In other instances the lower de- 
ciduous incisors may be absent. We recently saw a case of absence 
of the deciduous upper central incisors, with the space between 
the lateral incisors being occupied by only one peg-shaped tooth. 
The absence of teeth from the arch, (abnormalities of number) 
should be diagnosed invariably with the aid of carefully secured 
radiograms. Unquestionably, many cases of absence of teeth, as 
reported in the past, have been cases of noneruption or incarcer- 
ation of fully calcified teeth which had remained within the sub- 
stance of the jaws; in some cases this incarceration did not cause 





Fig. 222. — Noneruption of permanent Fig. 223. — Noneruption of permanent 

cuspid. cuspid. 

any apparent discomfort to the patient, while in others it pro- 
duced reflex manifestations of varying degrees of intensity. The 
third molar is often missing which is due almost invariably to 
its noneruption, and not to failure either of calcification of the 
tooth follicle, or to the evolution of the tooth germ. 

The series of cases of noneruption of the third molar which 
here follow belong to a class in which the presence of abnormal 
degrees of irritation in the jaws brought about severe nervous 
manifestations, reflex in character. The conditions encountered 
in these cases indirectly undermined the individual's health, 
for the reason that continued pain acts as a powerful source of 
inhibition from those nervous stimuli which are indispensable 
for the continuance of all vital functions. Pain, regardless of 



ABNORMALITIES IN THE NUMBER OF TEETH 



295 



its source, gives rise to functional disturbances proportionate to 
its degree of severity. Pain must be combated without delay 
because of its injurious effect upon the nervous function. So well 




Fig. 




Fig. 225. 

did Soullier, that scholarly therapeutist of Lyons, appreciate the 
significance of disturbed functional activity caused by continued 
degrees of pain, that he referred to this symptom as being to the 
nervous system what hemorrhage is to the vascular. 



296 



dental pathology 
Case Histories 



A young woman, twenty years of age, had been suffering intense pain 
for a period of several months. She had sustained a loss in weight of six- 



1 




w 




f 




wi 


■■* i 


HB 


t 



Fig. 226. 




Fig. 227. 

teen pounds in six weeks. This ease (Fig. 224) showed impaction of the 
upper and lower third molars. Their removal was followed by severe post- 
operative pain, but three weeks afterward she had regained her usual nor- 
mal good health. 



ABNORMALITIES IN THE NUMBER OF TEETH 



297 



A man about thirty-five years old gave a history of tic douloureux of fif- 
teen years' standing. The x-ray showed an impacted lower third molar on 
the right side, which was removed. Improvement followed. 

A woman gave a history of intense pain in the right ear of ten weeks' 
standing. The specialist to whom she was referred treated her for otitis 
media. As a measure of last resort, and in order to relieve the intensity of 
her suffering, a puncture of the drum was made, but without bringing about 
the much sought-for relief. The removal of an impacted right third molar 
(Fig. 225) brought about complete cessation of all symptoms in one week's 
time. 

A girl, aged seventeen years, with painful reflexes in the ear, had an un- 
erupted third molar removed (Fig. 226), resulting in a cure within six 
weeks' time. 

A young girl complained of intense pain in the eyes and in the ear, and 




Fig. 228. 



gave a negative history of painful symptoms in the teeth. She also exhibited 
intense mental and hysterical symptoms. The pain had been going on for 
a period of three years. The radiogram showed impacted upper and lower third 
molars on both sides. These teeth were extracted, and while there were 
marked postoperative disturbances, eventually she regained her normal health. 

A girl, aged nineteen years, with painful reflexes localized in the ear, had 
the upper and lower impacted third molars extracted, and recovery soon fol- 
lowed. 

Fig. 227 shows the mouth radiogram of a girl, aged seventeen, giving a 
history of severe facial pain. The second bicuspid and second molar had 
failed to erupt up to the age of seventeen, but eventually came through of their 
own accord. 



298 



DENTAL PATHOLOGY 



A woman, aged forty-five years, gave a history of recurrent dull pain 
on the right side of the face in the upper and lower teeth. The radiogram 
(Fig. 228) shows an impacted lower third molar, which was extracted. There 
followed a complete disappearance of the painful manifestations. As a side- 
light on the influence of pathologic condition of the teeth as regards defec- 
tive phonation, this patient exhibited a peculiar symptom: when she called 
for advice and treatment her voice was of a deep, sonorous, husky type. With 
the extraction of the offending tooth, the charm of the feminine voice re- 
turned. 



CHAPTER XVII 

HUTCHINSON'S TEETH AND OTHER SYPHILITIC 
STIGMATA 1 

Etiology. — The transmission of syphilis to the child in utero is 
responsible for the production of characteristic malformations in 
the permanent incisors, cuspids, and first molars, and in the de- 
ciduous second molars. Cavallaro 2 has investigated the dental de- 
fects in children with congenital syphilis, and his masterly work 
offers a basis for accurate deductions. He has collected a large 
number of cases bearing on the question, and comes to the con- 
clusion that unquestionably congenital syphilis produces charac- 
teristic malformations in the teeth. 

The tooth described by Jonathan Hutchinson when considered 
alone, can not be pathognomonic of inherited syphilis; but when 
present in conjunction with other denial abnormalities, and with 
ocular and auricular disturbances, it is practically without ques- 
tion that the subject so affected is a heredosyphilitic. 

The deformities of the teeth to which Hutchinson called at- 
tention are the semilunar defects in the incisal region of the 
upper central incisor. The tooth is narrower at the incisal edge 
than at the neck, is a smaller organ than the normal tooth, and 
is accompanied by hypoplasia of the cusps of the first molar. It is 
sometimes found in the upper laterals, the lower incisors, and ex- 
ceptionally in the cuspids (Fig. 229). The tooth is not always 
notched incisally upon eruption, but acquires that characteristic 
after it undergoes abrasion consequent upon mastication. The 
deformity is due to imperfect calcification of the incisal end of 
the middle lobe of the incisor, the structure occupying the site 
of the future notch being delicate and imperfect and readily 
disappears when the tooth is subjected to attrition (Fig. 230). 
The typical so-called Hutchinson's tooth is not, as a rule, 



1 \Ve are indebted to the writings of Joseph Cavallaro in the Dental Cosmos, vols. 1 
and li, for the basic facts in the preparation of this chapter. 

2 Cavallaro, Toseph : Syphilis in Relation to Dentition, Dental Cosmos, 1908, Nos. 11 
and 12; and 1909, Nos. 1 and 2. 

299 



300 



DENTAL PATHOLOGY 



Fig. 229. — TTutc 




Diastema. (Cavallaro.) 



Fig. 230.— Hutchinson teeth. Cuspal erosions of canines and molars. (Cavallaro.) 



HUTCHINSON S TEETH AND SYPHILITIC STIGMATA 



301 



observable after the thirtieth year, 3 since the mesial and distal 
lobes undergo abrasion, and the incisal edge becomes very nearly 
straight, although a semilunar marking may persist above the 




Fig. 231. — Hutchinson's teeth. Cuspal atrophy of canines and first molars. Sulciform 
erosions of lower incisors. Vertical grooves. Diastema. Cup-shaped erosions of the 
persistent lower left deciduous molar. (Cavallaro.) 




Fig. 232. — Multiple sulciform erosions, general, and involving the bicuspids. (Cavallaro.) 




Fig. 233. — Lingual aspects of preceding illustrations. Hutchinson's teeth. (Cavallaro..) 



3 Cavallaro, Joseph: Loc. cit. 



302 



DENTAL PATHOLOGY 



abraded incisal edge. It usually affects both central incisors, one 
central alone rarely being affected. Fournier, cited by Cavallaro, 
has reported a case of congenital syphilis in which the cutting edges 
of the upper central incisors, the lower central incisors, and one 
cuspid had "well-marked crescentic notches." The Hutchinson 
sign refers particularly to the semilunar or crescentic notch on 
the incisal edge in the upper or lower, or both, central and lateral 
incisors and cuspids. 

The dental apparatus may be affected in many other ways as 




Fig. 234. — Hutchinson teeth. Honeycomb erosions. (Cavallaro.) 

the result of nutritional disturbances induced by the presence 
or introduction of the syphilitic virus into the child (Figs. 231 
to 236). To this source, among many others, but not exclusively, 
may be traced the tardy decalcification of the deciduous teeth, 
and the correspondingly late eruption of their permanent suc- 
cessors; the absence of certain teeth, such as the upper lateral 
incisors, or the lower bicuspids; the development of a tooth in an 
abnormal location, i.e., under the tongue, in the maxillary sinus, 



HUTCHINSON S TEETH AND SYPHILITIC STIGMATA 



303 



in the hard palate, vomer, nasal fossae, sphenoid, inferior orbital 
margin, stomach, ovaries, and in dermoid cysts; supernumerary 
teeth; underdevelopment of the jaws; and V-shaped palate, cleft 
palate, and harelip. 4 

Cavallaro considers that the Hutchinson's semilunar notching, 
particularly of the incisors, is "pathognomonic of hereditary 
syphilis in at least 50 per cent of cases/' and as his opinion is 




Fig. 235. — Hutchinson teeth. Microdontism. (Cavallaro.) 




Fig. 236. — Complete congenital absence of teeth in the upper arch. (Cavallaro.) 

sustained by Pournier, whose experience as a syphilographer is 
far-reaching, statements to the contrary by observers of only 
limited experience should carry very little weight. Cavallaro 's 
conclusions here follow : 5 

"1. In heredosyphilitics the following various dental stigmata 
are found : erosions of the crown, cuspal erosion, and Hutchin- 
son 's teeth; white sulci; white marks; delay of development and 



4 Loc. cit. 

5 Cavallaro, Joseph: Syphilis in Relation to Dentition, Dental Cosmos, February, 1909. 



304 DENTAL PATHOLOGY 

eruption; dental infantilism; microdontism ; amorphism ; per- 
sistence of the deciduous teeth; anomalies of structure, shape, 
number, direction, arrangement and color; vulnerability of the 
dental system; ectopia (malpositions), total or partial absence 
of teeth, wearing away, premature caries, premature loss of teeth, 
spaces between teeth (diastema), and the following maxillary 
stigmata: malocclusion, defective articulation of the dental 
arches, prognathism, ogival palate and cleft palate. 

"2. The dental stigmata are the most frequent characteristic, 
being persistent and indelible among the stigmata of hereditary 
syphilis. 

"3. The erosions are systematic; they occupy the same level on 
homologous teeth, and a different one on teeth of a different 
order (showing their relative periods of calcification). Besides, 
they have a marked predilection for some teeth (Hutchinson's 
Erosion in the upper centrals, horizontal grooves in the lower in- 
cisors, and cuspal atrophy in the canines and first molars). 

"4. The dental stigmata do not belong exclusively to the sec- 
ond, but are also frequently found in the first dentition. Some 
cases of dental stigmata in the third generation have been re- 
corded. 

"5. The cup-shaped, or honeycomb, erosion on the deciduous 
molars, especially on the second, is very frequent. 

"6. The dental alterations as found in idiots, backward chil- 
dren, etc., represent a type quite different from those found in 
hereditary syphilitic subjects. Hutchinson's teeth, the systemic 
lesions, the horizontal grooves, dental infantilism, and the cup- 
shaped erosion in the deciduous molars, are peculiar to hereditary 
syphilitic subjects, while in idiots the vertical grooves are noted. 

"7. The dental stigmata are rarely found alone (we have ob- 
served only three out of fifty-six cases) ; they are generally as- 
sociated with other stigmata of the head or with other general 
concomitant stigmata. 

"8. A relationship between the factors of Hutchinson's triad 
(a syndrome of congenital syphilis — Hutchinson teeth, otitis 
media, and diffuse interstitial keratitis), especially between the 
dental and the ocular lesions, is very frequently found. 

"In fifty-six cases of dental lesions ocular lesions were found 
thirty-five times, and auricular lesions twelve times. 



Hutchinson's teeth and syphilitic stigmata 305 

"9. The anatomic and pathologic examination of the dental 
follicles of syphilitic teeth furnishes us with the following char- 
acteristic symptoms: constrictions, which clinically correspond 
to the cuspal atrophies; alterations of the enamel and dentin, in- 
terprismatic spaces, interglobular spaces, rounded islands, granu- 
lations due to an inhibitory disturbance which acted upon the 
tissues during the period of development. 

"10. In the dental follicles of macerated and doubtless syphi- 
litic fetuses the following alterations have been found: Endo- 
vasculitis, perivasculitis, hemorrhage and parvicellular infiltra- 
tion. 

"11. The Spirochete pallida is abundantly found in the dental 
follicle near the so-called dentinal cap, in proximity to the ves- 
sels, and in their walls. 

"12. The dental stigmata depend upon a general morbid 
cause, which manifests its inhibitory action during the period of 
development of the tooth, i.e., the second half of intrauterine life 
and the first months of extrauterine life. Such a morbid general 
cause can be only syphilis. 

"13. The presence of vascular alterations and of the Spirocheta 
pallida in the dental tissues leads us to believe that the dental 
stigmata are of syphilitic nature and not of indirect syphilitic 
origin only. 

"14. The dental stigmata are of great importance for the diag- 
nosis of hereditary syphilis, indicating the disease even before 
the appearance of other stigmata. 

"Hutchinson's teeth, the cuspal atrophy of the first perma- 
nent molar, the multiple systemic lesions of the second dentition, 
the multiple and systemic lesions of the first dentition, especially 
the cup-shaped erosions of the molars, are pathognomonic of 
hereditary syphilis. In twenty-three out of fifty-six cases Hutch- 
inson's teeth have been found. 

"15. The maxillary alterations, although frequently found in 
hereditary syphilitic subjects, do not possess an absolute diag- 
nostic value. 

"16. The specific treatment is always to be suggested in hered- 
itary syphilitic children with dental stigmata, even if these 
stigmata are found alone and unassociated with other syphilitic 
or dystrophic stigmata. 



CHAPTER XVIII 
DENTAL CARIES 

Historical Data 

The destruction of the hard tissues of the tooth, commonly 
called caries, or decay, has been the subject of considerable specu- 
lation as to its etiology and pathology in ancient, as well as com- 
paratively modern times. Scores of theories are on record in the 
literature of the subject, some writers having adhered to as many 
as two or three of them, all to be discarded upon the publication by 
W. D. Miller of his epoch-making writings on the production of 
caries in vitro. The Egyptian skulls of the period around 450 b. 
c. show no evidence of any systematized attempt having been made 
in those prehistoric times at filling cavities of decay, although 
a few skulls have been unearthed with gold incrustations in the 
occlusal surfaces, leading to the supposition that some of the an- 
cient Egyptians had some inkling as to the need of repairing by 
artificial means the destruction wrought by caries. By inference 
it may be concluded that not even the earliest of races were free 
from the ravages of dental decay. Hippocrates, a Greek physician, 
who lived some five centuries before Christ, thought that caries 
was a manifestation of "stagnation of depraved juices." This 
theory, or a modification of it, persisted for centuries, even up to 
the end of the eighteenth century. A certain phlegm under the 
roots of teeth was considered by him as the cause of caries. But 
particularly interesting is his statement that food debris is a 
cause of caries which attacks the weakest and less adherent teeth. 
As late as the latter part of the eighteenth century this theory was 
exploited by Bourdet (1757), by Benj. Bell (1787), and Serre 
(1788). 1 

Cornelius Celsus, the Roman physician, born some twenty-five 
years before the Christian era, was aware of the existence of a 
malady which caused the formation of cavities in the teeth. 



filler, W. D. : Microorganisms of the Human Mouth, S. S. White Dental Mfg. 
Co., Philadelphia. 

306 



DENTAL CARIES 307 

Scribonius Largus, a contemporary of Emperor Claudius, 2 in 
the middle of the first century was the author of a conception of 
caries which persisted for centuries : It was to worms which grew 
in the teeth and gnawed away their substance that the cause of the 
disease was attributed. The worm theory of caries was accepted 
and promulgated by Musitanus of Naples (1635-1714), Krauter- 
mann (1766-1854), and Ringelmann (1824). 3 In this connection 
Scribonius admonished that "there are those who pretend that 
the forceps is the only remedy for odontalgia. Nevertheless, be- 
fore resorting to this extreme measure, other means can be uti- 
lized.. When a portion of the tooth is decayed, I advise that it be 
scratched with the excavator (scalprum medieinale) . The opera- 
tion is not painful and the remainder of the tooth will render the 
same service as the whole tooth. If the pain persists, one should 
have recourse to collutories, to substances to be chewed, to fumiga- 
tions, to dentifrices." 

The art of filling teeth with metallic substances was unknown to 
the Romans; but, on the other hand, they advised filling the 
cavities with a powder made of the excrements of mice or the 
livers of lizards and covering the filling with wax. 

Archigenes, toward the end of the first century, was particularly 
concerned in devising remedies against odontalgia, and combina- 
tions to be introduced into carious teeth, doubtless to control the 
pain associated with pulpitis. 

Galen, a physician who lived in the year 131 A.D., and later on 
Acetious of Amida, in 550 A.D., believed that caries Avas caused by 
disturbances of nutrition which produced vicious humors which 
should be allowed to desiccate. Again, that caries was the result 
of an inflammation of the dentin was advanced by Galen, Eus- 
tachius (1574), John Hunter (1788), Joseph Fox (1806), and 
Thos. Bell (1831.) 4 The inflammation theory of caries was revived 
in 1889 by Heitzman, Bodecker, and Frank Abbott of New York. 

In the Middle Ages, Khazes, born in Persia in 850 a.d., thought of 
caries as a process similar to the understanding which they had at 
that time of the gradual destruction of bone (caries of bone). 
Rhazes knew that acids had a destructive action upon the teeth. 

2 Lemerle, L : Notice sur L/Histore de 1' Art Dentaire. 
3 Miller: Loc. cit. 
'Miller: Loc. cit. 



308 DENTAL PATHOLOGY 

Ali Abbas 5 about the year 1094, a.d., in a voluminous treatise of 
medicine, mentions a number of diseases of the teeth, with cor- 
rosion, or caries, among them. 

Avicenna (980-1037), a Persian physician, the author of the 
Canon, and recognized by his contemporaries as the ''prince" of 
physicians, attributed destructive action to the dentifrices of that 
time, claiming that their causticity injured the substance of the 
teeth. He also admonished his readers that the narcotics used 
for toothache injured the teeth. Avicenna formulated certain 
rules for the prevention of dental disease. He recommended that 
certain articles of food which he conceived as being capable of 
undergoing putrefaction be eliminated from the diet, viz., fish 
and milk; avoidance of too hot or too cold beverages, particu- 
larly one after the other; avoidance of chewing hard substances, 
such as bone or sticky foods, viz., figs and sweets; 'avoidance of 
meats which injure the teeth; avoidance of contrivances for pick- 
ing the teeth: and as a remedy against dental ills, rubbing them 
with honey and burnt salt. 

Abulcasis, the author of the Altasrif, a treatise on surgery 
which appeared at the beginning of the twelfth century, devotes 
several sections of the book to dental disease. 

Giovanni d' Arcoli (John Arculannus), professor at Bologna, 
studied the means of arresting the ravages of caries. He recom- 
mended cleaning the cavity with acids and filling it with sheets 
of gold. Arculannus was apparently the first to suggest the fill- 
ing of teeth with gold foil in the year 1450. In 1470 John Pla- 
tearius, professor at Pisa, revived the worm theory of caries. 
This was the theory accepted by Ryff, who lived in the latter part 
of the fifteenth century and died about 1571. Lazare Riviere 5 of 
Montpellier, professor of chemistry, also appears to have ad- 
hered to the worm theory of caries and recommended certain 
substances to destroy them. Ambroise Pare, a famous French 
physician and surgeon of the sixteenth century, discusses cer- 
tain diseases of the teeth in a book published in 1560; but his 
theories of caries are just as impossible as those of his prede- 
cessors, whose views we have already recorded. He leans to- 
ward the theory of vicious humors as expounded by Hippoc- 



6 Lemerle, L- ' Notice sur 1' Histoire de 1' Art Dentaire. 



DENTAL CARIES 309 

rates and Galen twenty and fourteen centuries, respectively, 
previously. 

Pierre Fauchard, a French dentist and writer who lived in the 
latter part of the seventeenth and the first part of the eighteenth 
century (1728), made efforts to find the worms that had been 
considered by his predecessors as the cause of decay, but he, as 
well as Pfaff, a German dentist (1756), failed to locate these 
animalcules, and abandoned the worm theory. Thereafter, to 
Fauchard, "caries was produced by a humor which finds its way 
into the osseous fibers of the tooth, or by a depraved saliva, or by 
rough foods, or by certain eroding substances placed upon the 
teeth to cure or bleach them. The internal causes are contained 
in the blood by making it less fluid and causing it to form ob- 
structions in the vessels of small diameter. The teeth are more 
subject to caries than the other bones of the body because their 
tissues are closer together, which explains their obstruction and 
strangulation." 

The putrefaction theory of decay was described by Pfaff, but, 
of course, we know now that a tooth may remain for any length 
of time in a putrefying mass without the enamel being thereby 
affected. The electrical theory of decay was also in vogue for 
some time, and was championed by Bridgeman before the Odon- 
tological Society of Great Britain in 1861. John Hunter (1728- 
1793), in his famous book published in 1771, in which he dis- 
cusses the anatomy and diseases of the teeth, admits that caries 
is a disease of obscure origin and not caused by external irrita- 
tion or chemical processes. 

Neither Jourdain (1734-1816), writer and dentist, nor Bourdet 
(1757), writer and dentist, added anything to the notions in 
vogue in those times concerning caries. Berdmore, in 1771, was 
the first to investigate the action of nitric and sulphuric acids 
upon the teeth ; to sour food and to acids an injurious action had 
been attributed back in 1677 by Pascti. One of the most pro- 
lific writers upon the subject of the chemical cause of caries was 
Magitot. Tomes, in 1873, reached the noteworthy conclusion 
that caries is the effect of external causes in which so-called vital 
forces play no part; and that caries is due to the action of acids 
that have been generated b} r fermentation in the mouth ; but at 
that time Tomes attributed no importance to the agencies through 



r 



310 DENTAL PATHOLOGY 

which this acid was generated in the mouth. In more recent times 
•Jonathan Taft was a strong advocate of the chemical theory. 
Magitot was able to produce artificial cavities in extracted teeth 
by the action of the products of the fermentation of sugar, as 
well as with several acids. The chemical theory alone, however, 
does not explain all the phenomena concerned in dental caries. 
The chemico parasitic theory, the one to which we adhere today, 
was brought out to some extent by Leber and Rottenstein in 1867. 
W. J. Milles and A. S. Underwood, in 1881, before the Dental 
Section of the International Medical Congress of London, reported 
in a paper on the "Nature of Dental Caries" the constant pres- 
ence of microorganism in tooth decay, and the widening of the 
tubules produced by microorganisms. Milles and Underwood 
should be credited with the first microscopic demonstration of the 
bacterial causation of dental caries. Their opinion was to the 
effect that the acid that dissolved the enamel was secreted by the 
bacteria. It remained for Miller to clarify the situation, which he 
did following a series of painstaking investigations resulting in 
the production of artificial caries in the laboratory identical in 
etiology and pathologic lesion with caries as it develops in the 
teeth of man. 

Miller's theory, as accepted today, is to the effect that caries of 
the enamel consists in its entirety of the dissolution of the enamel 
by lactic acid formed in situ by the fermentation of carbohydrates 
which adhere to the surface of the enamel; and that caries of den- 
tin and ccmentum consists of two distinct steps: (1) the dissolu- 
tion of the inorcjanic salts from these tissues, and, (2) a subsequent 
action by proteolytic bacterial enzymes upon the organic constit- 
uent of the dentin and ccmentum of the tooth. 



CHAPTER XIX 
DENTAL CARIES (Cont'd) 

General Considerations 

Dental caries is the most widely distributed disease of mankind. 
Peoples of all countries and races are subject to its ravages, and 
have been for all time, since caries lesions have been discovered in 
exhumed skulls of all ages. In some localities and among certain 
peoples it occurs with greater frequency and intensity than in 
others, but everywhere it is to be found. It lias been estimated that 
from 85 to 95 per cent of the people of the civilized races suffer 
from caries. 

There seems to exist a direct relation between the progress of 
civilization and the increase in the prevalence of dental caries. In 
the less civilized and barbaric tribes the prevalence of caries is 
small; in the highly civilized peoples the percentage rises tremen- 
dously. In prehistoric times the percentage of carious teeth varied 
from as low as 2 per cent, or less, to about 7 per cent; in contem- 
poraneous times, and among the most highly civilized people, par- 
ticularly, the percentage rises to 95 per cent and even higher. With 
the advance in civilization there has occurred a gradual, though 
radical change in the dietaries of men, and whereas, in prehistoric 
and ancient times the character of the food was such as to act as 
a cleanser or detergent of tooth surfaces, and as a stimulus to the 
growth of the jaws leading to regularity of position of the teeth in 
the arch, in modern times the food, being of the soft and mushy 
variety, has a tendency to become lodged upon the surface of the 
enamel, and affords little stimulation to the development of the 
jaws. The consequence is that the teeth are malposed in the arch 
and strongly predisposed to dental caries. Pickerill attributes the 
immunity to caries among the uncivilized tribes of the world not 
to an excessive protein diet and a small carbohydrate intake — for he 
tells us that the dietaries of the uncivilized tribes do not necessarily 
consist of protein substances only, but that they are decidedly of a 
mixed character. He attributes the immunity from caries to the 

311 



312 DENTAL PATHOLOGY 

use of salivary stimulants — fruits with their fruit acids, acid or 
pungent plants, sour foods, etc. — and masticatories, viz., gums of 
different trees which, when chewed, stimulate the flow of saliva and 
therefore increase diastatic action. No importance is attributed 
by Pickerill to the use of coarse fibrous foods as detergents in the 
case of the immune races, for again he assures us that in the case 
of the Maori, and other similar races, nearly all food is steamed, 
thus considerably reducing its toughness. Be that as it may, we 
are, however, satisfied that the character of the food per se is of 
paramount importance in maintaining the surface of the enamel 
free from the sticky coatings so evident in mouths of the caries sus- 
ceptibles. The views of Bunting 6 are here quoted in corroboration 
of the belief that the nature of the foods ingested has a bearing 
upon the production of dental caries. He says, "It is very evident 
that certain forms of carbohydrates have a greater tendency to 
stick to the teeth than others. The soft sticky varieties of sugars 
and cooked starches, which are slowly soluble, are especially liable 
to retention, and form favorable pabulum for acid fermentation. 
That the continued and copious diet of such substances is favor- 
able to caries can not be doubted. The mouths of candy-makers, 
millers, and children who eat largely of sweets, are strong in the 
corroboration of this view. And conversely, we know that the 
Eskimo and the meat-eating tribes of South America, who have 
little or no carbohydrate in their diet are, as a race, remarkably 
free from caries." 

The presence of salivary stimulants in the diet of the immune 
races, and their absence from the diet of the civilized races, un- 
doubtedly plays an important, but not exclusive, role in the deter- 
mination of susceptibility and immunity. Pickerill, whose investi- 
gations on the dietaries of the immune and susceptible races in their 
relation to dental caries constitute a most complete and depend- 
able study on the subject, traces the lack of immunity — the high 
susceptibility to dental caries — to dietaries which contain an 
abundance of food articles which act as salivary depressants and 
which are of high potential acidity. Some of his conclusions con- 
cerning the prevalence of caries among the civilized and uncivi- 
lized races are quoted here in further elucidation of the subject: 

1. That the number of persons affected with dental caries who 



6 Bunting: Journal of the National Dental Association. 



DENTAL CARIES 313 

live under uncivilized or "natural" conditions is comparatively 
small varying from 1 to 20.8 per cent, while in civilized modern 
races the percentage is as high as 98 per cent, the increase being 
at least 77.4 per cent. 

2. That the number of teeth affected with caries in each individ- 
ual is far less in those leading natural lives than in those leading 
artificial or highly civilized lives, in the former varying from 2 to 
7 per cent, while in the latter it has become as high as from 15 
to 52 per cent, showing a maximum increase of 45 per cent. 

3. That in the British races, which have been subject to the in- 
fluence of civilization for nearly 2,000 years, the increase in the 
percentage of caries is about 79 per cent. This corresponds 
closely to the difference in percentage given above in 1. 

4. That in the Maori race, which has been subject to the in- 
fluences of civilization for only seventy or eighty years at the 
very most, but has only become "civilized" in habits quite re- 
cently, the increase is 93 per cent. (But against this apparently 
high figure has to be set the fact that the incidence of caries in 
each mouth is comparatively low.) 

Caries is a disease which has kept up its ratio of increase witli 
advancing civilization. J. K. Mummery, 7 for instance, tells us 
that in the series of skulls of the primitive races examined 
by him the percentage which showed carious teeth varied from 
1.4 in the Eskimo to 20.8 in the negro (slaves) ; in the civilized 
races this ratio has increased tremendously. In English and 
Scotch school boys and girls, in a series of 10,500 individuals, 
the presence of carious teeth was found in 86 per cent of the 
cases; in the children of Leith the percentage was 98.60. The 
percentage among American school children, while not nearly so 
large as among European school children, is nevertheless alarm- 
ingly high. 

In a series of cases examined by Emerson, out of 1478 children 
from one to fifteen years of age, 81.2 per cent had carious teeth. 
In this percentage, namely 1200 children, 5996 decayed teeth 
were found, which is an average of 5.0 teeth for each one of the 
1200 children, or 4.7 teeth for each one of the 1478 individuals 
examined. These children were not suffering from any acute 
disease, although their general health was failing on account 



transactions of the Odontological Society of Great Britain. 



314 DENTAL PATHOLOGY 

of sickness during the winter previous to the examination, 
and also on account of various forms of malnutrition, anemia, 
and general debility, all doubtless traceable to the oral 
infection present. Of 634 cases over fifteen years of age, also 
in indifferent health, probably on account of unhygienic living, 
only 19, or 3.0 per cent, had no defective teeth; this leaves 615, 
or 97 per cent, in whom were found 4022 decayed teeth, or an 
average of 6.5 teeth for each of the 634 children examined. In 
this same group of 634 individuals, 1655 teeth were missing, and 
in addition 1444 artificial teeth were present, making a total of 
3099 teeth which had been presumably removed for advanced 
caries, or an average of 4.8 per cent for each one of the 634. 

There are so many factors which favor the development and 
progress of caries that where some are lacking, others are pres- 
ent to favor its progress. From the time a tooth makes its ap- 
pearance through the gum, and throughout the life of the in- 
dividual, it is exposed to the conditions which bring about caries, 
although, of course, there are periods when the teeth are more 
susceptible to caries than at others, as well as periods of com- 
plete, or almost complete, immunity. The amount and composi- 
tion of the saliva ; the position of the teeth in the arch and their 
relation to their antagonists; the structural peculiarities of the 
enamel and of the dentin; the character of the diet; the general 
health status; and the degree of hygienic care, if any — these 
alone or in combinations, are at the bottom of the caries problem. 
There was a time when it was assumed that cleanliness of the 
teeth was the most powerful and only weapon in the prevention 
of caries; but today Ave must conclude, in the face of observations 
that have been made in this and other countries, that the constitu- 
tional factor can not be altogether eliminated from the discussion 
of the subject any more than it can from pyorrhea alveolaris, 
or from diseases of the eye, throat, nose, skin, etc. These ob- 
servations concerned themselves with the marked tendency to 
dental caries in some months which were maintained at all times 
in a state of scrupulous cleanliness, as well as with the absence 
of caries in certain other instances of badly neglected mouths. 

The cliemicobacterial theory of Miller, promulgated by him in 
1882, has stood the test of scientific inquiry all this time ; and while 
it explains the modus operandi of dental caries with scientific 



DENTAL CARIES 315 

exactness, still, certain important phases of the problem of dental 
caries remain as yet to be explored. We know how a tooth decays 
in the presence of carbohydrate deposits upon its surfaces, with 
their subsequent fermentation, with lactic acid as the end-prod- 
uct; but we do not know why caries is rampant in some mouths 
and absent in others, under apparently identical conditions of 
health, diet, climate, living quarters, dental hygiene, etc. Is it 
the composition of the salivary secretion? The evidences ad- 
duced so far concerning the individual constituents of the saliva 
in the role of induction or prevention of caries, does not clear 
the question to any great extent. The sulphocyanate content, 
for instance, bears no relation to the subject, as shown by Gies, 
Howe, Bunting, and others. 

Bearing on the question of the immunizing properties of the 
saliva, Miller's studies throw considerable light on certain phases 
of the question, although with negative results. Considering a 
possible similarity between the hemolytic power of the blood 
serum and the substances which are introduced into the body 
when the individual is immunized, experiments were conducted in 
order to ascertain whether the saliva has any hemolytic action. 
These experiments show that fresh saliva brings about an im- 
mediate total solution of blood cells, but that this action is not 
due to any substance contained in the saliva, but to its water 
content, as proved by the fact that 0.75 per cent of sodium 
chloride, when added to the saliva (i.e., an isotonic saliva solu- 
tion), does not hemolyze the red blood cells of the rabbit. That 
the saliva has practically no antiseptic power whatsoever, has 
also been conclusively shown, inasmuch as microorganisms re- 
tain their virulence in the presence of human saliva. Miller also 
attacked the problem of caries immunity and susceptibility from 
the standpoint of the number of bacteria in the mouth, but his 
experiments show that the saliva of those immune to caries con- 
tains almost as many organisms as the saliva of those having 
moderate caries, or even those who are highly susceptible to the 
process. He says: "The saliva of immunes develops, in the 
presence of carbohydrates in and out of the mouth, on an average, 
a little less acid than that of highly susceptible persons. The 



316 DENTAL PATHOLOGY 

difference is, however, not constant, and is not sufficiently marked 
to account for the marked difference of susceptibility. ' ' 8 

This conclusion has been corroborated by Bunting, who like- 
wise found very little difference in the amounts of acids formed 
in the saliva of immunes versus that of susceptibles. Bunting 
expresses his conclusion by stating that the ability to ferment 
carbohydrates varies in different individuals, as well as in the 
same individual, but that this rate of fermentation bears no ap- 
parent relation to the caries susceptibility. 9 

The observations of Miller have been confirmed by Lothrop un- 
der the direction of Gies, the distinguished biological chemist 
of Columbia University. "The results obtained," says Lothrop, 
"show that there is acid production regardless of the condition 
of the mouth and teeth of the individual from whom the cul- 
ture was obtained." Further, as to whether the bacteria from 
susceptible mouths can extract more lime salts from the tooth 
than the bacteria from immune mouths, has also been the sub- 
ject of his investigation, and he has found that cultures of bac- 
teria from a case of perfect immunity extracted practically as 
much calcium as any culture from decay cases. 10 

The quantity of the saliva undoubtedly plays an important role. 
People with scanty saliva, almost dry mouths, and dry mouths, 
are more susceptible to the ravages of caries. This is probably 
due to the fact that in the presence of a scanty saliva the sur- 
faces of the teeth are not freed of sticky, starchy deposits and 
in superficial cavities the amount of saliva is not sufficient to 
dilute the acid products of fermentation, which remain in a con- 
centrated form, more rapidly dissolving the enamel. In more or 
less dry mouths food collects upon the surfaces of the teeth, 
and particularly in the interproximal spaces, remains undisturbed, 
undergoes fermentation, and soon the lactic acid end product dis- 
solves the enamel. 

But again, viscosity of the saliva, viz., whether it is watery or 
thick and sticky, does not seem to correspond in a constant way 
with susceptibility to, or immunity from, caries. A thick saliva 
has been found in mouths free from caries, and a thin secretion 



Wliller. W. D. : Dental Cosmos, xlv, 689. 

°Bunting: Bulletin ot the National Dental Association, October, 1914. 
10 Lothrop, Alfred P.: The Oral Microorganisms: A Bacterio-Chemical study of Den- 
tal Caries, Journal of the Allied Dental Societies. 



DENTAL CARIES 317 

in mouths in which caries was rampant, although, in the majority 
of instances in mouths in which the teeth are being rapidly disinte- 
grated through caries the saliva is thick and ropy, and, vice 
versa, a thin and watery saliva is secreted in mouths not so sus- 
ceptible to caries. 

Michaels found in the saliva a carbohydrate which he supposed 
to be glycogen, and supposed that the saliva of many individuals 
susceptible to dental caries contained such a carbohydrate. This 
view was controverted by Miller, although he was inclined to be- 
lieve that an acid fermentation of mucin is a possibility, and per- 
haps is accountable for the development of cervical caries. In 
recent years Gies, 11 after an exhaustive investigation into the 
composition of the saliva in its relation to the development of 
caries, has shown that the assumption that saliva may contain 
glycogen in sufficient amounts to become a factor in the produc- 
tion of caries is not supported by scientific evidence. But, on 
the other hand, his experiments with mucin, as carried out with 
the collaboration of Loewe, indicate that this glucoprotein dis- 
solves calcium from the tribasic calcium phosphate, and that 
it is highly probable that mucin is able to dissolve calcium from 
enamel. 

The foregoing considerations are intended for the purpose of 
preparing the reader for a discussion of the predisposing causes 
of dental caries. 

Predisposing Causes 

There are those conditions of the individual teeth or of their 
environment which favor the development of caries. The predis- 
posing causes are separate and independent from the exciting 
causes and, contrary to the latter, are not entirely external to 
the tooth. Hence, it is that liypoplastic defects of the enamel, 
either macroscopic or microscopic, and of the dentin; the amount 
and composition of the saliva; the position of the teeth in the arch; 
the overlapping of the teeth or having broad contacts; the diet 
as well as the age; the diameter of the bacterial flora; and the 
proper hygiene of the mouth and teeth — these are some of the fac- 
tors which may influence the development and progress of caries. 



"Gies, William T. : Biochemical Studies of Saliva and Teeth, Tournal of the Allied 
Dental Societies, 1914. 



318 



DENTAL PATHOLOGY 



Hypoplastic enamel defects predispose to caries in two ways: 
(1) by affording places of retention for food debris; and (2) 
by presenting areas of tissue lacking in normal protectiveness 
by reason of the absence or defectiveness of the interprismatic 
substance and of the enamel, or again by presenting areas 




Fig. 237. — Defective fissure in a molar. The dark area from a to a represents imperfect 
calcification. There were no external evidences of dental caries, although at b, decal- 
cification has started. There is lack of interprismatic substance in the dark area as well 
as between the enamel rods beyond the dark area. Probably as high a proportion as 
80 per cent of the fissures of permanent molars and bicuspids are defective. Invariably 
Nature's effort to close the fissure is accomplished by depositing an amorphous calcific 
mass in the bottom of the fissure. In this mass enamel rods are sometimes to be de- 
tected. 



of decreased enamel thickness. It is a rarity to find a perfect fis- 
sure in the molars and bicuspids, for surely at least nine out of 
every ten molars examined clinically and microscopically show 
plainly these defects (Fig. 237). No break may exist in the con- 
tinuity of the enamel in the apex of the fissure, while on the other 



DENTAL CARIES 319 

hand, these fissures may be so deep that they almost reach to the 
dentin at the dentoenamel junction and afford excellent me- 
chanical retention for fermentable food particles. In such loca- 
tions the acid end product (lactic acid) remains undisturbed and 
undiluted, and caries progresses more rapidly than in other loca- 
tions. The necessity for careful and frequent supervision of these 
teeth by the dentist with the purpose of arresting the caries 
process from its inception or, what is most to be preferred, of pre- 
venting it altogether, can not be too strongly emphasized in the 
minds of the laity. 

But defects in the enamel are not restricted to the fissures of 
bicuspids and molars, nor to pits in the lingual surfaces of in- 
cisors, nor to irregularities of surface in any of the aspects of a 
tooth. Predisposing causes are likewise to be found in defects 
due to insufficiency of structure; e.g., the chalky spots or those 
of different shades of brown, which are the result of the partial 
or almost complete absence of interprismatic (binding) substance 
with a low grade calcification of the enamel rods. A pit on the 
labial surface of an incisor is not, however, as a general rule, a 
location of choice for the onset of caries, for the reason that 
the enamel rods may be so disposed in the depression — in a mesh- 
like arrangement — as to offer a fair degree of obstruction to the 
action of the acid end product of carbohydrate fermentation. 

Teeth whose dentin has an abundance of interglobular spaces 
are predisposed to a wide spreading of caries, jlalposition of 
one, several, or of all the teeth in the arch predisposes to caries 
by favoring the lodgment and retention of fermentable food par- 
ticles. "The amount of foodstuffs," says Bunting, "which are 
retained about the teeth is in direct relation to the character 
and function of the masticatory apparatus. In case the dental 
arch is composed of well-formed and well-placed teeth, all of 
which are in good occlusion with their antagonists, the food may 
be finely divided, and finding no favorable place for lodgment, 
it will be washed out of the mouth and swallowed. Such a set of 
teeth may be said to be 'self-cleansing.' On the other hand, 
the poorly formed teeth and teeth which are irregularly arranged 
and in abnormal occlusion, tend to offer retention for foodstuffs, 
and are less likely to be self-cleansing. In the regular spaces 
between such teeth, in flat interproximal spaces, and in wedge- 



320 DENTAL PATHOLOGY 

or V-shaped areas formed by the overlapping of teeth, food will 
be wedged and retained until it has been either removed me- 
chanically or destroyed by bacterial action." 

In fact, any surface of any tooth which is inaccessible to the 
toothbrush or to friction during mastication is a favorite place 
for the onset of caries. The bearing of the diet on the develop- 
ment of caries, as has already been indicated, is obvious. The 
consumption in abundance of starchy and sweet foods is a strong 
predisposing factor of caries; and vice versa, a diet poor in 
these carbohydrates, but consisting of meats to a large extent, 
is conducive to restricted caries. Among the Guachos of the pam- 
pas of Argentina, who subsist mainly on meat, caries is prac- 
tically absent, while among the aborigines of Chile, where the 
diet is mixed, caries is present in a relatively large proportion. 
The Eskimos, certain meat-eating tribes of North American In- 
dians, Icelanders, and Lapps, are almost entirely exempt from 
caries. 12 

Age is a predisposing factor of caries to the extent that dur- 
ing the early years of life, and up to around the twentieth year, 
the greatest susceptibility to dental caries .exists mainly on ac- 
count of insufficient mouth hygiene by children and the young, 
and infrequent examinations by the dentist. Pregnancy is proba- 
bly a predisposing factor of caries, but exclusively by virtue of the 
neglect of brushing the teeth incident to the woman's general 
condition. That osteomalacia of pregnancy affects the teeth has 
never been proved; but, on the other hand, inflammations of the 
gingiva and gums, which occur during pregnancy, again by rea- 
son of neglect of the toilet of the mouth and teeth, predispose 
to caries by the loosening or retraction of these tissues from the 
neck of the tooth with the consequent exposure of the enamel 
near and at the neck of the tooth and of the cementum to the in- 
fluence of carbohydrate fermentation. The flabbiness and re- 
traction of the soft tissues around the necks of the teeth favor 
the retention of food particles. 

In the order of their importance the predisposing causes were 
listed by Miller as follows : 

1. The structure of the teeth [i.e., poorly developed, soft, porous 



'-Miller, W. D.: Loc. cit. 



DENTAL CARIES 321 

teeth, with many large (dentinal) [interglobular spaces] makes 
for a high predisposition to caries. 

2. Abnormally deep fissures or blind holes (foramina ceca) in 
molars and upper lateral incisors, especially in cases where the 
enamel also is poorly developed. 

3. Fissures and cracks in the enamel. 

4. Crowded or irregularly placed teeth. 

5. Recession or loosening of the gums. 

6. Pregnancy. 

7. Heredity. 

8. Various general diseases by imparting an acid reaction to 
the oral secretions, such as rheumatism, gout, diabetes, gastro- 
enteritis, dyspepsia, cancer of the stomach, scrofula, rachitis, and 
tuberculosis. 



CHAPTER XX 
PATHOLOGIC PROCESSES IN DENTAL CARIES 

Dental caries is a molecular disintegration of the hard tissues 
of the tooth by chemic abacterial agencies. It is a process whose 
etiologic factors are external to the tooth, and which consists 
of two distinct steps in the case of both dentin and cementum: 
Adz., (1) the disintegration of the inorganic matter by lactic 
acid, the result of carbohydrate fermentation, and (2) the destruc- 
tion of the organic matter by the action of peptonizing bacterial 
enzymes. The dissolution of the enamel, which is the first stage 
of caries, results from the fermentation of carbohydrate food 
by the direct action of bacterial enzymes. The enamel -con- 
taining only a minute portion of organic matter, its disintegra- 
tion occurs exclusive of any peptonizing action. The enzymes of 
mouth bacteria possess the property of splitting monosaccharides 
into lactic acid. The starches are acted upon in the mouth by the 
amylolytic enzyme, ptyalin, and converted into maltose, a disac- 
charide. The starches taken into the mouth as food have the 
general formula (C 6 H 10 O* 5 ) x, the x standing for an unknown 
multiple. The action is one of hydrolysis, and may be expressed 
as follows: 

Starch 

2C 6 H 1U 5 -f HX> + ptyalin = C u H a O M (maltose). 

C 12 H.„0 lt -f- H,0 -j- bacterial enzyme = 2C 6 H 12 O a (glucose, or dextrose). 

This conversion of starch into maltose takes place in different 
steps: 

1. Starch, which gives a blue color with iodine. 

2. Soluble starch or amylodextrin, which gives a blue color 
with iodine. 

3. Erythrodextrin, which gives a red color with iodine. 

4. a — Acroo dextrin (no color with iodine). 

5. (3 — Acroo dextrin (no color with iodine). 

6. y — Acroo dextrin, and possibly other dextrins. 

7. Maltose. 

322 



PATHOLOGIC PROCESSES IN DENTAL CARIES 323 

Maltose, C 12 H 22 11 , becomes hydrolyzed in the presence of one 
molecule of water into C 12 H 24 12 and, bacterial enzyme being avail- 
able, this is split into glucose (dextrose) 2C 6 H 12 G , which again, in 
the presence of a bacterial enzyme, is split into lactic acid, to wit : 

2C 6 H 12 6 = 4C 3 H 6 3 (lactic acid). 

The degrees of fermentation of certain carbohydrates by bac- 
teria have been exhaustively investigated by Gies and Kligler. 1 

"Glucose was fermented by practically all the strains secured 
from dental deposits. Lactose and sucrose were attacked less 
regularly, though by larger majorities of these strains. The bac- 
terial strains tested by the authors in this series of investigations 
numbered four hundred and twenty-six. The accompanying 
table embodies the result of these investigations. 



GLUCOSE 

SUGARS GircosE GLUCOSE GLUCOSE LAC ™ SE 

FERMENTED GLUC0SE LACT0SE SUCR0SE ONLY ,^° ™° SUCR0 SE 



LACTOSE SUCROSE 



INDIVID- 
UALLY 



Number of bac- 
terial strains 
tested 426 386 326 426 3S6 326 322 

Percentage of 
the strains 
that induced 
fermentation 99.5 70 72 1.3 23 16 56 



"The relative fermentability of certain sugars in equivalent 
volumes by typical oral bacteria, as measured by the resultant 
amounts of acid, has also been determined by Gies and Kligler. 

"The test media were made from meat infusions according to 
the standard methods and included the addition of one per cent 
of the sugar to be tested. The titrations were made w T ith N/ 20 
sodium hydroxide solution, phenolphthalein serving as the in- 
dicator. The results as expressed in the following table are 
in terms of the number of cubic centimeters of normal hydroxide 
solution necessary to neutralize 100 c.c. of the culture medium, 



1 Chemical Studies of the Relations of Oral Microorganisms to Dental Caries, Journal 
of the Allied Dental Societies, December, 1915. Because of the scientific value of these 
observations they are quoted in full with the consent of Professor Gies. 



324 DENTAL PATHOLOGY 

each value representing average acidity produced by the dif- 
ferent representatives of a given species under approximately 
equal conditions of incubation of each form : 



TYPE OF 
ORGANISM 


GLUCOSE 


SUCROSE 


MALTOSE 


LACTOSE 


D. flavus 


2.5 


2.6 


2.7 


0.6 


Staphylococcus 


4.5 


2.5 


3.1 


4.5 


Streptococcus 
B., acidophilus 
C. placoides 
L. buccalis 


4.2 
5.6 
3.2 
3.9 


4.2 
0.9 
4.3 
0.5 


5.4 
3.7 

2.7 


4.0 
5.8 
0.5 
0.4 


Actinomyces 


1.9 


0.2 


0.4 


0.6 



"According to Kligler the recently isolated strains of staphy- 
lococci, streptococci, and bacillus acidophilus, represent the 
most active acid-producers. The average results of the staphy- 
lococcus are 4.8, streptococcus 4.8, and B. acidophilus 7.0. 

"It appears from the foregoing experiments that glucose and 
maltose are more rapidly fermented in general than sucrose and 
lactose, also that the amounts of acids produced from the sugars 
used were fairly constant in most cases for each type of bacteria. 
The B. acidophilus is capable of elaborating and withstanding a 
greater amount of acid than that produced and resisted by any 
of the other types." 

It is well to remember in connection with the process of car- 
bohydrate fermentation, as bearing upon the production of 
dental caries, that we have to deal with monosaccharides or sim- 
ple sugars, disaccharides or double sugars, and polysaccharides 
or multiple sugars. The monosaccharides, C (1 H 12 6 , are directly 
split by bacteria into C 3 H O 3 (lactic acid). The monosaccharides, 
or hexoses, are the sugars found in fruits, honey, and in sugar 
of milk as a derivative of lactose. These are glucose, dextrose, 
and grape sugar, levulose, fructose, and galactose. Dextrose, lev- 
ulose and galactose are fermentable by yeasts and by any num- 
ber of bacterial enzymes such as are constantly present in the 
mouth. 

Glucose is a thick syrup obtained from corn starch by the ac- 
tion of dilute sulphuric acid. The corn starch and dilute acid 
are heated together, the acid first converting the starch into 
grape sugar. The excess of acid is removed by treatment with 



PATHOLOGIC PROCESSES IN DENTAL CARIES 325 

chalk. The filtered solution is either evaporated to syrup and 
sold as "glucose" or evaporated to dryness and sold as grape 
sugar (Simon). 

Dextrose is found in honey. Levulose and fructose occur in 
sweet fruits and honey, and galactose in sugar of milk. 

The disaccharides or saccharoses comprise principally the sug- 
ars obtained from cane sugar (saccharose), from beet sugar (sac- 
charose), and from milk (lactose). Their general formula is 
C 12 H 22 1:L . In the process of hydrolysis one molecule of the disac- 
charide takes up one molecule of water and splits into two mono- 
saccharide molecules, thus C 12 H 22 O xl + H 2 = 2C G H 12 G . To the 
list of disaccharides should be added maltose and isomaltose — 
end products in the hydrolysis of starch. 

The polysaccharides are starch, glycogen, dextrin, inulin and 
cellulose. It is with starch that we are distinctly concerned in 
the study of dental caries. This polysaccharide is insoluble in 
cold water, alcohol, and ether. It comes in the form of an amor- 
phous, white, tasteless powder, or in masses. It is unabsorbable 
as such, but must first be hydrolyzed into maltose and then into 
dextrose through the action of an organized or unorganized en- 
zyme, in either case the intermediate products of the hydrolysis 
being the same. Starch is widely distributed in nature, being 
found in the seeds of cereals and leguminosas, and in the stems, 
roots and seeds of nearly all plants. From starch down to the 
production of lactic acid the chemical reactions involved are ex- 
pressed as follows: 

STARCH Maltose 

2C,H 10 O 5 + HX> -f ptyalin = C^H^O^ 

Maltose Dextrose 

C^H^Oj! + HX> -f maltase enzyme = 2C H ]2 O t; . 

Dextrose Lactic Acid 

2C c H 12 O fi + B. enzyme = 4C.,H.O„. 

The dissolution of the interprismatic substance or of the enamel 
rods, or of both, is followed by the penetration into the dentinal 
tubules of the acid end product of fermentation and of bac- 
teria which have the power of dissolving (peptonizing) the or- 
ganic matrix of the dentin. As the enamel is penetrated and the 
decalcifying agent reaches the dentoenamel junction the process 
spreads laterally with a rapidity proportionate to the prominence 



326 



DENTAL PATHOLOGY 



of the granular layer. The more marked the latter ; i.e., the greater 
the size of the expansions into which the tubules open, the more 
rapid and greater will be the lateral involvement at the dento- 
enamel junction. 

The area of involvement at the dentoenamel junction, because 
of the facility with which bacteria will travel along this line, is 
greater than the area of involvement in the dentin toward the 
pulp. It is for this reason that the carious process in the dentin 
assumes a conical shape or, as expressed by Black, the tendency is 
to the formation of a conical area of decay with the point of the 
cone toward the pulp of the tooth and its base at the dentoenamel 
junction (Fig. 238). In the presence of wide tubular expansions 



f f 




L^ f^% 




m j 




w% 




.. ^m JSi 


w *'Nlf 






W' ■ 







Fig. 238. — Typical conical form of penetration of caries into the dentin; the base of 
the cone is at the dentoenamel junction while the apex of the cone is toward the pulp. 
(G. V. Black.) 



at the dentoenamel junction — the granular layer — the amount of 
calcined matter to be acted upon by lactic acid will be proportion- 
ately decreased, so that caries will advance rapidly and a greater 
area of underlying dentin will become involved. Caries in a fis- 
sure, after the dentoenamel junction has been reached, and when 
an excessive granular layer is present, will advance more quickly 
laterally than in deptli into the dentin, and this lateral caries will 
then advance toward the enamel undermining the enamel cap over 
a considerable area. 

The calcium salts of the dentin are dissolved by the lactic acid 
and the remaining tough, cartilaginous matrix is then acted upon 
by peptonizing bacterial enzymes. The bacteria penetrate the 



PATHOLOGIC PROCESSES IN DENTAL CARIES 



327 




Fig. 239. — Microorganisms in the structure of the dentin. (Miller.) 




Fig. 240. — Microorganisms in the structure of the dentin. (Miller.) 



328 DENTAL PATHOLOGY 

dentinal tubules as soon as access to them is secured by the dis- 
solution of the overlying enamel (Figs. 239-242). Here they can 
be seen in considerable numbers and occasionally the tubules ap- 
pear distended, evidently as the result of the action of the or- 
ganisms upon the decalcified or quasidecalcified structure of the 
tubules. Black was of the opinion that microorganisms do not 
penetrate into the dentinal tubules until the calcium salts have 
been dissolved for a short distance in advance of the bacteria. 

If, now, decalcification should proceed in an external direction 
from the dentoenamel junction, and coincidentally in an internal 
direction into the dentin, a cavity of considerable size will be 
formed having a very small opening externally. The lateral prog- 
ress of caries at the dentoenamel junction is designated as 
lateral caries, and the progress of caries from the lateral involve- 
ment back into the enamel is backward caries. The tendency for 
caries to spread rapidly as above described is not the case in all 
instances, as the decalcification of the enamel and dentin, and 
liquefaction of the organic dentin matrix, may be a slow process 
from the beginning — a long time elapsing until a fair-sized cavity 
is formed. The involvement of the dentin, unless proper treat- 
ment by filling is instituted, will continue until most of the 
crown is broken down. If the decay advances along the dento- 
enamel junction and from there several paths of decalcification 
develop into the enamel and the dentin, the support to the ename, 
rods is removed and these will soon break down, the top of the 
crown will collapse, and the enamel rods will be washed away 
by the saliva. The decay advances toward the pulp, in some cases 
painful symptoms developing as the result of pulp irritation, 
while in others no painful manifestations occur until such time 
as it is too late to save the pulp or even the tooth. 

The formation of lactic acid in the deeper structures of the 
dentin is explained by the late G. V. Black on the basis of os- 
mosis and dialysis. The sugar, as it is formed in the mouth by 
the fermentation of starches, or the sugars that are taken into 
the mouth as food and are there split into simple sugars, are 
dialyzed into the deeper structures of the dentin. Here they are 
further split into lactic acid by the bacterial enzymes of such 



PATHOLOGIC PROCESSES IN DENTAL CARIES 329 




Fig. 241 — Microorganisms in the structure of the dentin. (Miller.) 




Fig. 242. — Microorganisms in the structure of the dentin. (Miller.) 



830 DENTAL PATHOLOGY 

bacteria as have previously penetrated into the tubules, or which 
are in the deeper layers of the decalcified dentin matrix in prox- 
imity to as yet sound dentin. By the same process of dialysis 
the inorganic salts of the dentin which combine with lactic acid 
to form calcium lactates or calcium lactophosphates, find their way 
into the saliva. 



CHAPTER XXI 

CARIES OF THE ENAMEL 

Etiology and Pathologic Anatomy- 
It develops upon the enamel in spots or areas which favor the 
attachment of bacteria which, as the resnlt of their activity in 
a carbohydrate medium, produce lactic acid. This dissolves first 
the interprismatic substance between the enamel rods, and then 
the rods themselves. This incidence is easily demonstrated upon 
free fragments of enamel when the dissolution of the inter- 
prismatic substance by lactic acid or any other acid brings into 
view the outlines of the individual enamel rods by establishing a 
greater margin of difference between the reflectiveness of the 
rods and that of the interprismatic substance, the rods standing 
separated from each other at their free ends (Fig. 243). 

The bacteria which induce the fermentation of carbohydrates 
upon the surface of the enamel are supposed to become collected 
under a protecting gelatinous mass which the late G. V. Black 
and J. Leon Williams have considered to be essential in the de- 
velopment of caries. These coatings of gelatinous consistence, 
designated by Black as gelatinous plaques, were by him inter- 
preted as the product of bacterial activity. The slimy deposits 
which form upon the surfaces of the teeth, particularly during 
sleep and in the mouth not properly cared for, are not the 
plaques described by Black. The mucinous plaque is not the 
result of the precipitation of mucin, as thought by many, for 
the reason that mucin precipitates in the form of flakes which 
do not adhere to the enamel. The formation of the plaque from 
mucin is a purely physical process. Black considered the plaque 
as an essential factor in the retention of bacteria upon tooth sur- 
faces and also in the localization of the products of carbohydrate 
fermentation. The plaque is not, however, considered by Kirk 1 
as essential in the progress of caries, and again, Hopewell-Smith 



^irk, E. C. : A Consideration of the Question of Susceptibility and Immunity to 
Dental Caries, Dental Cosmos, 1910, xli, 729. 

331 



332 



DENTAL PATHOLOGY 



is of the opinion that the mysterious plaque is nothing more than 
fragmentary remains of Nasmyth's membrane. Gries has sug- 
gested the use of weak solutions of organic acids as mouth washes 
and mouth cleansers on the assumption that the precipitation of 
mucin in flakes, and their consequent elimination in the saliva, 
would prevent the formation of the mucinous plaque. Bunting tells 
us that the plaques and films which form upon the teeth are not 
of the same character in their composition. He says that some 




Fig. 243. — Artificial decalcification of the enamel by one ycr cent hydrochloric acid sim- 
ulating caries, a, dentin; b, sound enamel; c, artificially decalcified enamel. 



forms of plaque which occur in certain mouths have the property 
of favoring caries and making it possible, while in other cases 
films are formed which are protective in their nature and which 
do not favor acid fermentation in their substance. 

The disappearance of the cementing substance leads to the 
falling and washing away of the enamel rods (Fig. 244). The 
first symptom of caries of the enamel is a whitened spot pro- 



CARIES OF THE ENAMEL 



333 




Fig. 244. — Caries of enamel at the deepest portion of the cavity. In the dentin, the 
lightest area at a, is the transparent zone of Tomes. At b, in the transparent zone 
tubular calcification had not been so marked. A wall of enamel at c, surrounds the 
cavity shown at d; a mass of decalcified broken-down enamel is shown at e, f, g, and h. 



334 DENTAL PATHOLOGY 

duced by the dissolution of the cementing substance. Here the 
enamel feels chalky and soft to 'the explorer. Localization of 
caries of the enamel is, in the order of frequency, in the follow- 
ing areas of the tooth: 2 

1. (a) Pits or fissures in the occlusal surfaces of bicuspids and 

. molars. 

(b) In the buccal surfaces of molars. 

(c) In the lingual surfaces of molars. 

(d) Occasionally the lingual surfaces of the upper incisors. 

2. In the proximal surfaces of all the teeth. 

3. In the gingival third of the buccal or labial surfaces of all 

the teeth, and rarely in the lingual surfaces. 

Certain discolorations upon the approximal surfaces of molars 
and bicuspids are probably the result of the penetration of a 
slightly decalcified enamel by extraneous substance from the 
saliva. The discolorations in fissures of bicuspids and molars is 
attributed by Hopewell-Smith to color changes in a persisting 
Nasmyth's membrane by certain microorganisms, to wit: B. 
nuorescens liquefaciens. 

In occlusal surfaces caries develops in fissures and pits because 
here the friction of mastication is unable to keep these locations 
clean. Once food debris becomes lodged in a pit or fissure, it un- 
dergoes fermentation, with the result that the interprismatic sub- 
stance and rods are dissolved. The occlusal surfaces are sub- 
jected to considerable friction during mastication. The lingual 
surfaces of the upper and loAver teeth are kept clean by the fric- 
tion of the tongue, and the buccal surfaces are likewise main- 
tained in a relative degree of cleanliness by the friction of the 
cheeks and lips. As a general proposition it may be said that the 
beginning of caries is located in areas which are not ordinarily 
subjected to friction, either by the cheeks, lips, tongue or during 
mastication. Seldom, if ever, do the prominent lines of a tooth — 
those which are frequently cleaned by either muscle friction, the 
toothbrush, or the food itself during mastication — become the 
original seat of caries. Rather, it is the points on the surfaces of 
teeth that offer a place of concealment for food or bacteria that 
are first attacked in caries. The process of caries is limited by the 



2 Black, G. Y. : Pathology of the Hard Tissues of the Tooth, vol. 



CARIES OF THE ENAMEL 



335 



position of normal gum tissue, by friction in mastication, by mus- 
cle friction, and by artificial cleaning. 




Fig. 245. — Caries of enamel in proximal surfaces. It has progressed in the direction 
of the enamel rods. All of the dark area (marked X) is carious enamel, the decalcifica- 
tion having affected the interprismatic substance, which is practically dissolved away, 
the individual rods can be distinguished without difficulty. The area marked E is sound 
enamel. In this specimen caries had progressed part way through the enamel. (G. V. 
Black.) 



In the approximal surface caries of the enamel exhibits a tend- 
ency to follow the lengths of the enamel rods, but this is by 
no means a constant tendency. Many a microscopic section re- 



336 



DENTAL PATHOLOGY 



veals the fact that caries is likely to progress across the long 
axis of the rods after a certain area of enamel has become de- 
calcified (Figs. 245 and 246). In pits, also, the progress is oc- 
casionally across the lengths of the rods (Fig. 247). 

The pit may not show externally any evidence of caries, but 
upon examination the explorer will detect an opening, and caries 




Fig. 246. — Caries of enamel in a proximal surface in which caries has made consid- 
erable progress. D, dentin, J:, enamel (sound), X, carions enamel, the dentoenamel 
junction is seen between D and IS. (G. V. Black.) 

will be found to have penetrated the thickness of the enamel 
and to have spread across the lengths of the enamel rods toward 
the dentoenamel junction. 

In proximal surfaces the predisposing cause of caries is to be 
found in the failure of the septal tissues to completely fill the 
interproximal space. Under normal conditions the septal tis- 



CARIES OF THE ENAMEL 



337 



sues will fill this almost to the contact point, and the food glides 
over them so that none, or only very small particles, becomes 
lodged under them. Under conditions which bring about inflam- 
matory disturbances of the septal tissues, causing them to recede, 
food becomes lodged in the spaces and caries begins there, be- 
cause that portion of the enamel which was previously protected 
is now exposed to the influence of carbohydrate fermentation. 

In pits and fissures caries advances frequently across the 
lengths of the enamel rods. The outline of the caries process in 
these localities is more or less conical, with the apex of the cone 




Fig. 247. — Caries of enamel in a pit. The whiteness in the enamel around the pit 
is caused by the dissolution of the interprismatic substance. Caries has advanced across 
the long diameter of the enamel rods. (G. V. Black.) 



at the bottom of the pit or fissure, and the base at the clento- 
enamel junction (Figs. 248 and 249). In these cases it is not 
unusual to find the enamel thoroughly undermined, with the 
opening into such a cavity very minute. Food which accumu- 
lates in a pit or fissure is not readily disturbed, so that any 
acid produced there by the fermentation of carbohydrates has 
ample time to dissolve the rods even before the dentin has been 
penetrated, because it remains slightly diluted, being not readily 
washed away by the saliva. 

A strong predisposing cause of caries in the approximal surfaces 
of incisors is to be found in an inflammation of the septal tis- 
sues. Their natural rounded form is destroyed, or the tissue 



338 



DENTAL PATHOLOGY 



shrinks from its normal position, — in either event producing a 
space between the septal tissues and the approximal surfaces of 
the teeth in which food accumulates and undergoes fermentation. 
The incidence of caries here is usually in a very small spot, the 
whitened surface of the enamel marking the location at which 




Fig. 248. — Progress of enamel caries in a molar. The dark area represents the portion 
of the enamel that has been decalcified by the lactic acid end-product of carbohydrate 
fermentation, a, dentin; b, b, dentoenamel junction; c, partly decalcified enamel; d, com- 
pletely decalcified enamel, c, sound enamel; f, interior of cavity. 

the cementing substance has been dissolved away. Then the 
advance of caries is exactly the reverse of what occurs in pits 
or fissures; that is to sny, the penetration is in the shape of a 
cone with the base on the surface and the apex toward the dento- 
enamel junction. The central portion of the cone is in close 



CARIES OF THE ENAMEL 



339 



proximity to the dentin, and it is there that the dentin is first 
affected by the acid of caries. 

The tendency in the approximal surfaces of bicuspids and 




Fig. 249. — Progress of enamel caries in a molar. A greater enlargement of the same 
section shown in Fig. 247. 

molars is for the carious process to begin at some point and 
spread in a buccal and lingual direction. Spreading toward the 
occlusal is apparently the exception. 3 

3 Black, G. V.: Operative Dentistry, i. 



CHAPTER XXII 
CARIES OF DENTIN AND CEMENTUM 

Etiology and Pathologic Anatomy 

Following the decalcification of enamel by the acids which 
result from the fermentation of carbohydrates, the dentin be- 




Fig 250. -Caries of dentin showing decalcification of the organic constituents and 

conversion into a soft cartilaginous mass, a, pulp chamber; b, b, decalcified dentin which 
has been converted into a soft cartilaginous mass. 

comes involved. In the dentin conditions are present which make 
for a difference from the process of caries in the enamel. The 
decalcification of the dentin — that is to say, its conversion into 

340 



CARIES OF DENTIN AND CEMENTUM 



341 



a tough cartilaginous substance — is designated as the softening 
of the dentin (Figs. 250 and 251). It is the result of the dissolu- 
tion of the inorganic salt constituents of the tissue. This soft 




Fig. 251. — Caries of dentin showing decalcification of the inorganic constituents and 
conversion into a soft cartilaginous mass; a, interior of cavity; b, decalcified dentin 
which has heen converted into a soft cartilaginous mass. 

mass may be easily peeled off, and when compressed, discharges 
a small quantity of liquid of a strong acid reaction (Miller). 



342 



DENTAL PATHOLOGY 



The softening of the dentin is followed by a partial or complete 
liquefaction of the organic matrix. This organic matrix is the 
cartilaginous substance which remains after decalcification has 
been effected and which upon disintegration or liquefaction leads 




Fig. 252. — Undermining caries; destruction of tooth substance from within. (W. D. 

Miller.) 



to the formation of a cavity. Decayed dentin may be of any 
shade from the natural color to black. 

The progress of decay in dentin, as pointed out by Miller, fre- 
quently assumes the outline of a Florence flask and the over- 
lying undermined enamel often breaks under the pressure of mas- 
tication. In microscopic sections the enamel is seen separated 



CARIES OF DENTIN - AND CEMENTUM 



343 



from the underlying dentin. Caries in some cases proceeds 
rapidrr at the dentoenamel line. In some cases the caries 
process advances in the shape of a narrow canal directly to- 
ward the pulp. These cases are designated as penetrating 
caries. The lateral spreading of caries in the dentin at the 
dentoenamel junction, or the progress toward the pulp, is 
governed by developmental conditions. In fully developed 
teeth, with many interglobular spaces at or near the dentoenamel 




Fig. 253. — Undermining caries; destruction of tooth substance from within. (W. D. 

Miller.) 



junction, the decay spreads rapidly on all sides under the enamel; 
when teeth are dense the decay travels in the direction of the 
dentinal tubules toward the pulp. In some cases, in the molars 
and bicuspids, there will be externally a relatively slight indica- 
tion of caries while the crown of the tooth may be thoroughly un- 
dermined (Figs. 252, 253 and 254). As a rule, however, as the 
cavity in the dentin increases, the enamel at the opening becomes 
disintegrated and collapses upon the slightest pressure, inas- 



344 



DENTAL PATHOLOGY 



much as unsupported enamel easily breaks off. The progress of 
caries in the dentin is more rapid than in the enamel. The pu- 
trefaction of meats in a cavity through its alkaline end products 
may lead to the neutralization of the acids of fermentation, with 
the arrest of caries, but the caries may begin anew should 
starches or sugars replace the putrefactive material. 

The two phenomena which must be considered in connection 




Fig. 254. — Undermining caries of approximal surface; undecayed enamel cusp (a) about 
to break away. (\Y. 1). Miller.) 

with dentin caries are (1) transparency, and (2) pigmentation, 
or discoloration of the decayed tissue. 

Transparent Zone or Zone of Tomes 

In carious dentin a transparent area between the pulp and the 
limiting line of the decayed portion is usually to be seen in mi- 
croscopic sections, but not always, the latter condition being 
probably due to the unfavorable plane in which some sec- 
tions are cut. "When present, this phenomenon is designated 



CARIES OF DENTIN AND CEMENTUM 



345 



as the diaphanous lialo, or the transparent zone of Tomes (Fig. 
255). This area of transparency is present in the dentin which 
has not as yet become involved in the carious process because of 
the preponderance of inorganic salt content, as compared with ordi- 
nary dentin thereby offering greater resistance to decalcifying 
agencies (Fig. 256). It has the form of a cone with the apex to- 
ward the pulp, the axis of the cone following the direction of the 
tubuli. Miller found that the cone is bounded on each side by an 




Fig. 255. 



-Caries of dentin. At b is shown the decayed area while at a is shown the 
transparent zone of Tomes. (W. D. Miller.) 



opaque band. At least three hundred specimens of decayed teeth, 
which had been worn down, mounted on opposing plates were 
examined by him, and in no instance was any transparency found. 
Further, this phenomenon is not exclusively an accompaniment 
of caries. It is observed in sound teeth which have been worn 
off by abrasion or erosion, and in senile teeth where the roots 
in their entirety frequently become transparent. Miller observed 
the transparency in the teeth of old dogs which had undergone 



346 



DENTAL PATHOLOGY 



abrasion. The true cause of this transparency has not yet been 
definitely established, but several things have been definitely 
proved, namely, first, that it does not occur in devitalized teeth 
undergoing caries ; second, that decalcification has not taken place 
in the transparent area, as proved by differential quantitative chem- 
ical analysis ; third, that microscopic examination of the transparent 
zone shows an increase in the thickness of the walls of the den- 
tinal tubules within the transparent zone, with a corresponding 




Fig. 



256. — Transparent zone of Tomes in dentin; it offers greater resistance to de- 
calcifying agencies than normal dentin. (W. D. Miller.) 



decrease in the size of the dentinal fibrillar ; and fourth, that chemical 
analysis shows a greater proportion of lime salts in the transparent 
area. The area of transparent^ is in all probability due to an 
increase in lime salts, with a consequent thickening of the walls of 
the tubules and a corresponding decrease in their diameter which 
results in an equalization of the normally different indices of 
refraction of the tubules and of the calcified dentin matrix. 
The transparent zone is therefore the result of the stimula- 



CARTES OF DENTIN AND CEMENTUM 347 

tion of the odontoblastic layer of the pulp, for the odontoblasts 
preside over the deposition of additional lime salts in the walls 
of the tubules. This increase in the amount of calcified tissue 
protects the pulp against the ravages of caries by rendering less 
rapid the decalcification process and by establishing a barrier to 
the thermal insults to the pulp which follow a loss of enamel 
structure, even in a small area. 

Pigmentation 

Every degree of discoloration of the dentin may be observed 
from the normal color of the tissue to a yellow, yellowish brown, 
dark brown, or black. The first appearance of decay is not 
characterized by any visible discoloration neither is it present 
in acute caries. But it is present in chronic, slow-developing 
caries, and hence it may be said that the intensity of discoloration 
is in inverse ratio to the length of time of the involvement. Dis- 
coloration of the dentin is not exclusively a phenomenon of decay 
but occurs also whenever dentin is laid bare. Discoloration in 
worn off teeth is frequently the ease in both smokers and non- 
smokers. The same phenomenon is observed in the teeth of dogs. 
That the discoloration arises from without, and is not a phenom- 
enon of dentin caries, strictly speaking, is the prevailing opinion 
among investigators. It has been variously explained by the ac- 
tion of acids upon dentin; by the color-forming power of bacteria; 
and Black has explained it by the settling of coloring matter de- 
rived from the action of hydrogen sulphide upon such metallic 
elements as may be introduced into the mouth. Miller attributes 
discoloration to the action of microorganisms upon organic mat- 
ter. W. H. 0. McGehee 1 has found that practically all the color- 
ing agents or dyes which are used by manufacturers for coloring 
dentifrices, stain tooth structure. This investigator was able to 
stain enamel, dentin and cementum in the laboratory with a ma- 
jority of dentifrices on the market. Tooth structure was likewise 
stained in the course of his laboratory experiments by dentifrices 
which did not contain added coloring matter or dyes, the pig- 
mentation in these instances being due to the ingredients in the 
dentifrices which possess color. The stains were found to be pene- 

*McGehee, W. H. O. : Dental Cosmos, March, 1912. 



348 



DENTAL PATHOLOGY 



trating, and not to be affected by sunlight or continued washing. 
Clinically it was found by the same experimenter that vital teeth 
in the mouth are occasionally stained by the use of colored denti- 
frices. It was brought out that nonvital teeth stain much more 
readily than vital teeth, and that "vital and nonvital dentin and 
cementum, whenever exposed, readily take almost any stain 
with which they come in contact, as they are found discolored in 
practically every instance in which they have been exposed for 





Fig. 257. — Caries of enamel and dentin 
which beginning on the mesial surface has 
progressed beyond the enamel-cementum 

junction and involved the cementum and 
underlying dentin. 



Fig. 258. — Caries of cementum on la- 
bial surface of abraded upper left central 
incisor. 



any length of time;" and further that "cracks in the enamel, 
abraded and eroded surfaces, cavities of decay, and other similar 
conditions, offer excellent evidence of stains of every character." 
McGehee condemns the use of colored dentifrices, his experi- 
ments having shown that when constantly used they will stain 
the tooth structure. 

In connection with the study of dentin caries it should be 
noted that the average diameter of a dentinal tubule is greater 
than that of most of the bacteria found in the mouth, and conse- 



CARIES OF DENTIN AND CEMENTUM 349 

quently it must be inferred that bacteria find their way into normal 
tubules, regardless of any previous decalcification of their walls. 

The Decay of Cementum 

The inorganic portion of the cementum becomes decalcified by 
the action of the acid end product of fermentation, and this is 
folloAved by the liquefaction of the remaining organic matrix 
(Figs. 257 and 258). It occurs when the peridental membrane 
has been detached from the cementum, food becoming lodged in 
the pockets so formed. The invasion occurs along Sharper *s 
fibers. 



CHAPTEE XXIII 
HYPERCEMENTOSIS 

General Considerations 

Hypercementosis, hypertrophy of the cementum (or dental ex- 
ostosis, as it is sometimes erroneously called) is an increase of 
cementum substance which serves no physiologic purpose. It 
is observed in the teeth of the young, as well as in those of the 
adult, and while it may not cause any reflex painful symptoms, it 





Fig. 259. — Hypercementosis of lower Fig. 260. — Hypercementosis in upper 

first bicuspid and deflection of its root. right second molar. 

may, on the other hand, be the etiologic factor of serious nervous 
manifestations. The cementum is not a self -reproducing tissue: 
it is built upon the dentin from the dentoenamel junction to the 
apex on all the aspects of the root by the follicular wall, which is 
also the source of the alveolar process which serves to retain the 

350 



HYPERCEMENTOSIS 



351 



tooth. The follicular sac persists throughout the life of the tooth 
as the peridental membrane, the latter retaining the function of 
building or tearing down cementum when normal or pathologic 
conditions demand it. 






Fig. 261. — Hypercemen- Fig. 262. — Hypercemen- 

tosis in upper bicuspid. tosis of root of lower mo- 

lar — the two roots are 
united by a band of ce- 
mentum. 



Fig. 263. — Hypercemen- 
tosis involving the three 
roots of an upper molar. 




Fig. 264. — Hyperce- 
mentosis involving the 
apical area of the three 
roots of an upper molar. 



Fig. 265. — Excessive hy- 
percementosis in a lower 
molar. 



Fig. 266. — Excessive hy- 
percementosis in a molar 
which rendered its removal 
difficult and entailed the 
fracture of the surrounding 
alveolar process. 



Hypercementosis may affect only the apical portion of a root or 
roots of a tooth (Figs. 259-264) ; it may affect practically the 
entire root area of the roots of a molar or bicuspid (Figs. 265- 



352 



DENTAL PATHOLOGY 



268); or only one root or two roots of a triple-rooted molar; and 
it may be localized upon some portion of the root in the form of 
a nodule (Fig. 269). 




Fig. 267. — Hypercementosis involving the three roots of an upper left first molar. 




Fig. 268. — Hypercementosis of the posterior Fig. 269.- — Nodular form of hy- 

root of the lower first molar. percementosis. 



Etiology and Pathologic Anatomy 

A tooth root which is the seat of hypercementosis has a peri- 
dental membrane which for a prolonged period of time has been 
continuously subjected to a degree of irritation not strong enough 
to cause degeneration in the cells of the peridental membrane, 



HYPERCEMENTOSIS 



353 



and yet strong enough to cause a productive stimulation. An ir- 
ritation from any source which will cause unrecoverable degener- 
ations of the cells of the peridental membrane can not and will 
not result in hypertrophy and hyperplasia of the cementum. 
Therefore inasmuch as in hypercementosis there does occur an 
increase in the thickness as well as in the number of cementum 
lamellae, we are led to consider the process not merely as an hy- 
pertrophy, but as a combination of both processes, viz., hypertro- 
phy and hyperplasia. The cause of hypercementosis may be 




Fig. 270. — Resorption of dentin and obliteration of the resorbed area by cementum. 



mechanical, as for instance the pressure against the root of an 
adjoining tooth caused by the efforts at eruption of an impacted 
tooth; tooth movement in orthodontia ; the effect of pressure upon 
the roots of an impacted tooth by the unyielding character of 
the surrounding osseous structures ; the presence of a particle 
of root filling beyond the apical foramen through continued 
stimulation of the peridental membrane; the pernicious thread- 
biting habit ; the stimulation of the peridental membrane in- 
directly from the gingiva by the rough and protruding edges of 
fillings, or by salivary or subgingival calculi ; or undue stress of 
occlusion upon one or several teeth when the result is several 



354 



DENTAL PATHOLOGY 



hypercementosed teeth in the same mouth. Hypercemen- 
tosis is also observed where a root whose peridental membrane 
has been the seat of a chronic inflammation caused by very mild 
infection which has spread from the pulp; and while the inflam- 
mation may have brought about the destruction of a limited area 
of peridental membrane, it has also stimulated the cementoblasts 



































c 

d 

b 

a 














C 














d 

b 




















r 


*\\ 




a 



Fig. 271. — ITypercementosis accompanied by dentin resorption and filling in of the 
resorbed area of dentin by cementum. a, normal dentin; b, c, outline of observed dentin 
area, cementum of repair containing vast numbers of lacunae with their respective canalic- 
uli radiating toward the peridental membrane. 



in the adjacent healthy peridental membrane. In those cases of 
hypercementosis in which the hypercementosed area is involved in 
a chronic dentoalveolar abscess, the hypertrophy started at a time 
when the infection was of such a degree of mildness as to act as 
a regenerative factor — a stimulus. After the hypercementosed 
area was formed, the adjacent peridental membrane became the 



HYPERCEMENTOSIS 355 

seat of destructive changes upon the infection's acquiring 
greater virulence. It is thus that we account for a hypercemen- 
tosed apical root area in juxtaposition to a chronic dentoalveolar 
abscess (dental granuloma) . In chronic peridental inflammation 
in connection with pyorrhea alveolaris, hyper cementosis may 
develop in root areas even beyond those from over which the 
peridental membrane has been destroyed. It may also develop 
consequent upon the removal of the pulp when it may be the 
result of frequent and often needless manipulations with root 
canal instruments beyond the apical foramen, or as the result of 
the action of concentrated chemical disinfectants, or again fol- 
lowing a mild infection of the periapical peridental membrane. 
Anatomically, hypercementosis manifests itself by an increase 
in the number and size of cementum lamellae and occasionally 
by areas of dentin absorption next to the cementum with the sub- 
sequent tilling thereof by cementum (Figs. 270 and 271). 



CHAPTER XXIV 

ABRASION AND EROSION 

The results of abrasion and erosion, which differ in etiology, 
are clinically identical. It may be possible to distinguish by im- 
plication between them, but not exclusively on the evidence 
afforded by an eroded tooth surface or by an abraded one. By 
carefully investigating the forces of occlusion, both normal and 
pathologic; the character of the lateral contact of one tooth 
with another; the use of tough or coarse foods; the effect of 
extraneous forces upon the teeth, such as from pipe stems, 
the toothbrush, cigarette holders, thread-biting — a differential 
diagnosis between the two processes may be established. But not 
so on a clinical examination of the tissues themselves regardless 
of the influences of environment. Abrasion is a purely mechan- 
ical process; but erosion is either a purely chemical or a chemico- 
mechanical process. 

Etiology of Abrasion 

In abrasion of the crowns of teeth and, under certain circum- 
stances, of the roots, when these are exposed, portions are worn 
away producing surfaces with a high polish over which the end 
of an explorer will glide smoothly, resembling no other lesion of 
the enamel or dentin except erosion resulting from chemicome- 
chanical action. The teeth suffer from restricted degrees of 
abrasion from the time they assume their respective positions in 
the arch and begin to exercise their physiologic functions (Fig. 
272). When this abrasion is the result of the forces of masti- 
cation and occurs in teeth in more or less normal alignment, and 
the diet does not habitually contain coarse or gritty foods in ex- 
cessive amounts, it can be considered as a physiologic process. It 
is a pathologic process when it results from the continued friction 
between the surfaces of opposing teeth in malocclusion, when the 
result of undue friction by the toothbrush, or when because of the 
use of gritty tooth powders, or masticatories such as chewing 
gum or tobacco, or of holding pipe or cigarette stems between the 

356 



ABRASIOX AND EROSIOX 



357 



teeth. The loss of the posterior teeth, throwing the bulk of the 
force of mastication upon the anterior teeth, will in time bring 
about marked abrasion or wearing away of the occlusal surfaces 
of the anterior teeth. 

Pathologic Anatomy of Abrasion 

The shape of the abraded surfaces will depend upon the posi- 
tion of the tooth in the arch and the direction and extent of the 
frictional forces. It may be nothing more than a decrease in the 
vertical diameter of an incisor with the formation of a square 
area as the result (Figs. 273. 274. and 275) ; or it may have pro- 
gressed to the extent of a complete wearing away of the crown of 




Fig. 272. Abrasion — mechanical wearing away of the cusps of a lower molar. 

the tooth and a portion of the root (Figs. 276-279). Mechanical 
appliances, such as lingual bars, clasps, etc., are frequently the 
cause of abrasion. Such instances are seen in Figs. 280 and 281. 
Abrasions which resulted from abnormal stress of occlusion are 
seen in the series from Fig. 282-289. Any tooth may suffer from 
abrasion of such severity as to result in the disappearance of all 
of its crown and even a portion of its root. The abraded surface 
presents a highly polished appearance, and. regardless of the ex- 
tent of tooth structure lost, the pulp does not become exposed. 
since a constructive and protective process takes place simul- 



358 



DENTAL PATHOLOGY 



taneously with the loss of tooth structure. Tubular calcification 
and secondary dentin are going on constantly in teeth which are 
undergoing abrasion, and even in those extreme cases in which all 
of the crown and a portion of the root have been worn away the 




Fig. 273. — A scries of incisors which have suffered from slight abrasion. At a and b 
the dentin has been exposed consequent upon the wasting away of the enamel, labially 
and lingually, and has assumed a brownish yellow color. 




Fig. 274. — Abrasion of the incisal edges of two upper central incisors; brownish dis- 
coloration of exposed dentin. 



remnant of pulp tissue will be protected by secondary dentin. 
The pulp may also become the seat of degenerative changes, the 
calcific form being the most frequently encountered. 



ABRASION AND EROSION 



359 



Etiology of Erosion 

It had been assumed that erosion was a purely chemical proc- 
ess until the late W. D. Miller, after years of painstaking in- 
vestigations and experiments in the laboratory, was unable to 
produce the characteristic erosion facet by the action of acid sub- 
stances alone. He was able, however, to duplicate in the labo- 
ratory the typical erosion surface, with its high polish, by a com- 



















Pf-"^ 




b 


b 






























w 






























a 




















a 












Kft 














t ' 






^ 1 










c 

d 


c 




»v "v- 

























Fig. 275. — Photomicrograph of ground section of one of the abraded teeth shown in 
Fig. 274. a, enamel; b, dentin; c, abraded enamel with a chip broken off in mounting, on 
right side of picture; d, abraded and discolored dentin. 



bination of acid and mechanical action (Fig. 290). He therefore 
reached the conclusion that at least the experimental form of 
erosion was not entirely the result of chemical action. Any acid 
which is capable of abstracting calcium salts from the enamel and 
dentin, or of dissolving the interprismatic substance, may be con- 
cerned in erosion ; any acid or acid substance which is sufficiently 
powerful to disintegrate the organic basic substance of the dentin 



360 



DENTAL PATHOLOGY 



may cause wasting (erosion) with a minimum of mechanical 
action. 1 

In a case of extensive erosion studied by Kirk 2 lactic acid ap- 
peared to be the cause of the wearing away of the surfaces of 
the teeth; and in other cases studied by him he has attributed 




Fig. 276. — Upper right 
cuspid. Practically the en- 
tire crown has wasted away 
on account of abrasion. 



Fig. 277. — Upper cuspids which for many years had 
been the seat of abrasion. The entire crown in each 
case wasted away without exposing the pulp. 



the cause to the action of acid sodium phosphate and acid calcium 
phosphate, which are secreted by the gingival glands as the 
manifestation of a nutritional disorder. This nutritional dis- 



tiller, W. D. : Experiments and Observations on the Wasting of Food Tissue, Dental 
Cosmos, xlix, No. 2. 

2 Kirk, E. C: Items of Interest, xxiv, No. 7, July, 1902, p. 511. 



ABRASIOX AXD EROSION 361 

order is responsible for the presence in the blood of an excess of 
carbon dioxide which changes the basic sodium and calcium 
phosphates into their respective acid salts. 





Fig. 278. Fig. 279. Fig. 280. 

Fig. 278. — Abrasion of lower third molar. Complete wasting away of the crown. 

Fig. 279. — Abrasion of lower third molar. Complete wasting away of the crown. 

Fig. 280. — Spiral-shaped abrasion in upper left cuspid caused by an ill-fitting clasp. 
The wearing down of the hard tissues advanced beyond the boundaries of the pulp cham- 
ber which was filled with secondary dentin. 




Fig. 281. — A series of abraded lower cuspids, upon their lingual aspects, the result of 
continuous friction by ill-fitting clasps and lingual bars. 

Kirk states that in those disorders which are classified as dis- 
eases of sulfoxidation, the blood is loaded with an excess of carbon 



362 



DENTAL PATHOLOGY 




Fig. 282. — Abrasion of 
upper right central incisor, 
the result of an abnormal 
frictional stress consequent 
upon malocclusion; exposed 
and discolored dentin. 



Fig. 283. — Abrasion of 
lingual surface of upper 
left cuspid reaching beyont 
the pulp chamber; second 
ary dentin was depositee 
in sufficient amount to kee] 
the pulp protected from ex 
tenia! injury. 



Fig. 284. — Abrasion of 
the labial surface of the 
lower right first bicuspid. 




Fig. 285. — Cup-shaped abrasion in lower molars, the result of abnormal frictional stress 
consequent upon malocclusion. 



ABRASION AND EROSION 



363 



dioxide. "The excess of carbonic acid in the blood is to a certain 
extent taken care of in the excretory cells of the kidneys by the 




Fig. 286. — Cup-shaped abrasion in lower first molar, the result of abnormal frictional 
stress consequent upon malocclusion. 




Fig. 287.— Cup- 
shaped abrasion in a 
lower molar, the re- 
sult of abnormal 
frictional stress con- 
sequent upon maloc- 
clusion. 



Fig. 28S. — Cup-shaped abrasion 
in lower molar, the result of ab- 
normal frictional stress conse- 
quent upon malocclusion. 




Fig. 289. — Abrasion in 
a deciduous molar, re- 
tained in the arch long af- 
ter the normal time for 
its exfoliation. 



mass action of carbonic acid upon the sodium phosphate of the 
blood, thus: 

H 2 C0 3 + Na 2 HP0 4 = XaHC0 3 + NaH 2 P0 4 






364 



DENTAL PATHOLOGY 



The acid sodium phosphate is separated by the kidneys and 
carried off in the urine, the sodium bicarbonate being returned 
to the blood plasma, which is thus made to retain its alkalinity." 




IIPPI ) 



Fig. 290. — Action of acid calcium phosphate in conjunction with friction during two and 
one-third years. (W. D. Miller.) 




Fig. 291. — Tubular calcification in the dentin. This phenomenon is found in connection 
with caries, erosion or abrasion. ( \V. 1). Miller.) 

In the event of the carbonic acid being produced in proportions 
greater than normal the conversion of the basic sodium phos- 



ABRASION AXD EROSIOX 365 

phate into the acid sodiuni phosphate also takes place in the 
buccal glands, so that their acid exudate erodes the surfaces of 
the teeth. 

Pathologic Anatomy of Erosion 

The eroded surfaces may be shallow, irregular, saucer-shaped, or 
wedge-shaped. The eroded area has a highly polished and dense 
surface, and the process may involve the enamel, the dentin, 
and in some instances also the cementum. The eroded surfaces 
are usually located upon the labial and buccal surfaces, rarely 
upon the lingual. They are. as a rule, markedly sensitive, al- 
though again a thorough tubular calcification (Fig. 291) under the 
eroded area may cut off the tubules from the pulp, rendering 
the area absolutely insensitive. Calcification of the dentinal tubules 
and secondary dentin are constant accompaniments of erosion 
to a greater or less extent, and there may also occur degenera- 
tive changes in the dental pulp leading to atrophy. 



CHAPTER XXV 

THE SALIVA 
Normal and Pathologic Considerations 

The saliva is the mixed secretion of the three paired salivary 
glands — the parotid, sublingual and submaxillary — and of all the 
small aiveolotubular glands of the mucous membrane of the floor 
of the mouth, the palate, cheeks and inner lining of the lips. 

Amount: Salivary Stimulants and Depressants. — The amount 
of saliva secreted in twenty-four hours is variable among in- 
dividuals and for each one under varying conditions of diet, ex- 
ercise, temperature, habits, etc. ; it has been estimated at from 
500 to 1200 cubic centimeters. The secretion is influenced by 
direct or indirect stimulation, which may be normal or pathologic. 
The smell of a meal in the course of its preparation and the 
noise incident thereto, the sight of a succulent dish, the mas- 
tication of an appetizing morsel, etc., are common instances 
of indirect and direct stimulation. On the other hand, the 
salivary secretion is pathologically stimulated by inflamma- 
tions of the mucous membrane of the mouth (the several forms of 
stomatitis),* and by drugs such as pilocarpine, physostigmine, 
iodine and its compounds, mercury and its compounds, (which are 
specific sialogogues), acting by direct stimulation of the secreting 
cells of the glands. All acids, ethereal bodies, pungent 
substances, tobacco, nauseants, such as ipecacuanha, tartar emetic, 
are reflex sialogogues. They act by producing reflex dilatation 
of the glandular vessels through their action on the lining of the 
mouth. 1 In certain nervous disorders, as, for instance, during 
epileptic attacks, the salivary secretion is abundant. In the 
course of dental operations secretion of saliva is in some individ- 
uals markedly increased. It is the result of reflex stimulation, 
via the mucous membrane, by mechanical contrivances and be- 
cause of the pressure upon the parotid glands by the overlying 
tissues in the act of forcibly opening the mouth. The pres- 



*At the climax of an infectious inflammation of the mucous membrane of the mouth 
(stomatitis), the salivary secretion may be decreased rather than increased. 

1 Preston, C. II.: In N. G. Bennett's Science and Practice of Dental Surgery. 

366 



THE SALIVA 



367 



ence in the mouth of ragged teeth and of carious cavities is also 
a source of reflex stimulation of the salivary secretion. In dis- 
eases of the hypoacid diathesis characterized by lymphatic en- 
largements, in chronic follicular tonsillitis and tuberculosis the 
flow of saliva is abundant. 2 

Sialorrhea or an excessive flow of saliva, may be an accompani- 
ment of toxemias and febrile disturbances. 3 Dryness of the 
mouth (xerostomia), however, is not a rare occurrence in con- 
nection with febrile disturbances of some standing. Pain in the 
teeth produces an increased flow of saliva. The amount secreted 
by the parotid is less than one-third of the amount secreted by 
the submaxillary and sublingual together, and may be as low 
as one-twentieth or one-thirtieth. Acid substances produce 
greater secretion than SAveet substances. 4 

Color 

While saliva may be colorless, grayish or whitish, Michaels has 
observed that this may vary in certain pathologic states, while in 
others its normal color is not altered. The saliva of individuals 
of the hypoacid diathesis is colorless; that of the gouty and of 
diabetics is grayish. On standing the "saliva assumes secondary 
colorations" which are caused by oxidations and ammoniacal fer- 
mentations of organic substances contained in the saliva, mainly 
biliary elements. The following table after Michaels is in itself 
sufficiently explanatory: 

Different Colors Assumed by Human Saliva Upon Standing, and the 

Sources Thereof 
Normal Pigments 

Pigments which produce it. 
Biliverdin 



Color 
Greenish 
Yellowish 

Blackish green 
Bluish 
Brownish 
Dark brown 
Bed 

Golden yellow 
Black 



Abnormal Pigments 



Biliflavin 

Biliprasin 

Bilicyanin 

Bilifuchsin 

Bilihumin 

Bilirubin 

Urobilin 
Melanin 



2 Michaels, J. B.: Siaolo-Semeiology Transactions Fourth International Dental Con- 
gress, St. Louis. 1904. 

'Howe: Dental Cosmos, January, 1911. 
4 Pickerill: Oral sepsis. 



368 DENTAL PATHOLOGY 

The saliva, after it is poured on a watchglass, must be ex- 
amined with an oblique light, the rays striking the fluid from 
above downwards. 

The color assumed by the saliva on standing corresponds, in 
Michaels' opinion, to certain pathologic states. Thus, in gouty 
eczema the saliva assumes a greenish color; in indicanuria, a 
bluish color; in chorea, a brownish color; in rheumatism and 
oxaluria, a golden yellow color ; and in carcinoma, a blackish color. 
Normal saliva is a semitransparent, frothy fluid the aspect and 
consistence of which varies according to the proportion it con- 
tains of ptyaline, glycogen, mucin and inorganic salts. Michaels 
has stated that the saliva, if left in a bottle for some time, suffers 
a change in its consistence. In salivas containing cholesterin 
there is formed, after the specimen stands for some time, a thick, 
greasy, cream-white coating which floats on the surface. This 
characteristic is often found in the saliva of diabetics. "In the 
normal state the sediments occur in small amounts and are whit- 
ish. In those suffering hepatic insufficiency, the sediment ap- 
pears brownish ; in cancer patients, it is blackish. The sediment 
is composed of epithelial cells and fibrinous substance, and in a 
few hours falls to the bottom of the vessel." ( Michaels.) 

Odor 

Regardless of the odor which results from fermentation proc- 
esses in the saliva, or lactic and butyric fermentation in indi- 
viduals of the hypoacid diathesis, certain peculiar odors are char- 
acteristic of certain diseases. And so it is that Michaels connects 
a garlic-like odor with phosphorous poisoning, an ethereal odor 
with diabetes, an acetonic odor with diabetes and alcoholism, etc. 



Taste 

The taste of the saliva, which is insipid in normal individuals, 
is, for instance, bitter in disorders of digestion with hepatic in- 
sufficiency, sweet in diabetes, salty when soluble chlorides are 
present in the blood in excess of the normal, and metallic in 
chronic poisoning with mercury, copper or lead. 



THE SALIVA 369 

Constituents of the Saliva 

Organic 



(a) Mucin. 

(b) Ptyalin. 

(c) Proteins. 

(d) Potassium sodium and ammonium sulpliocyanids. 



Inorganic 



(Calcium phosphate. 
Calcium carbonate. 



Calcium bicarbonate (in fresh saliva), 



Potassium chloride, 
(b) Salts of Potassium { p otassilim phosphate. 



(c) Salts of Sodium 



Sodium chloride. 
Sodium phosphate. 
Sodium carbonate. 
-Sodium bicarbonate (in fresh saliva), 

J Magnesium phosphate. 
I Magnesium carbonate. 



(d) Salts of Magnesium 

(e) Salts of Ammonium j Ammonium carbonate. 



Summary 

The composition of the saliva may be summarized as follows: 
Water 994.90 

Organic matter 3.60 

Inorganic matter 1.50 

The secretion contains epithelial cells which have been thrown 
off by the epithelium of the mouth, and salivary corpuscles de- 
rived from the lymphoid tissue of the faucial, lingual, and pharyn- 
geal tonsils ; but these have no relation to the salivary glands. On 
entering the mouth these corpuscles swell and their protoplasm be- 
comes granular. 

Mucin 

The source of mucin is from the submaxillary gland and the 
mucin secretions of the mucous membrane. It is precipitated by 
weak acid solutions, e.g., acetic and lactic acids and by acid salts. 
It is the probable material of which the so-called "plaques" are 
composed, but not as the result of chemical precipitation. It 



370 DENTAL PATHOLOGY 

undergoes alkaline decomposition through the action of mouth 
organisms, and may be regarded under certain conditions only 
as an agent which protects the enamel, 5 for Gies has shown that 
the result of the fermentation of mucin has a dissolving power 
upon tricalcium phosphate. But, on the other hand, the mucin 
is not deposited by itself alone on the surfaces of teeth. Through 
its viscosity or stickiness it binds carbohydrate material to the 
teeth and soft tissues and the bacteria enmeshed in the mass bring 
about the fermentation of the carbohydrate material with the ul- 
timate production of lactic acid, the dissolving agent of enamel 
interprismatic substance and rods. Consequently, even should the 
mucin undergo putrefactive decomposition with the formation of 
alkaline end products, these are soon neutralized and rendered 
valueless as protective agents in the presence of acid substances 
when in amounts sufficient to counteract this alkalinity and also 
to dissolve the enamel structure; this, because the proportion of 
fermentable material exceeds by far the amount of the mucin in 
the slimy coatings or deposits. 

It may be precipitated not only by weak acids, but also by acid 
salts, such as acid potassium tartrate, and acid sodium phosphate 
(Kirk). Eopy saliva, in which this "ropiness" or "stickiness" 
is due to the relatively high mucin content, is associated with 
progressive caries in children and young persons. The source 
of mucin, to the extent of 80 per cent of its volume, is from the 
mucous membrane muc in-secreting glands, and the proportion 
of salivary mucin has been found by Vulpian to be as high in 
one healthy man as 0.32 per cent. 

Ptyalin 

Ptyalin is an amylolytic enzyme, because it possesses the 
property of transforming complex carbohydrates, such as starch 
and dextrin, into simpler bodies. When the amount of ptyalin 
is inadequate, the digestion of starch in the mouth is slow and the 
intermediate products, the dextrins, help to bind the starchy 
mass to the teeth. The microorganisms contained in the mass 
cause the fermentation of the enmeshed carbohydrates, with the 



5 Pickerill, H. P.: Prevention of Dental Caries, and Oral Sepsis, S. S. White Dental 
Mfg. Co., Philadelphia, 1914. 



THE SALIVA 371 

production of lactic acid, which arrests the action of ptyalin and 
decalcifies the enamel. 6 

The ptyalin index of normal resting saliva is increased more 
than tenfold by acid stimulation (Pickerill). The transforma- 
tion of starch into the end product maltose is by a process of 
hydrolysis, effected by ptyalin, the intervening products being 
erythro-dextrin, a-achroo-dextrin, /?-achroo-dextrin, isomaltose 
and finally, maltose. The action of ptyalin (salivary amylase) 
is arrested in the presence of even a trace of free acid, as weak a 
solution as 0.003 per cent having that effect. It acts best in a 
neutral or slightly alkaline solution. The digestion of starch by 
ptyalin in the stomach continues for about forty minutes or 
longer after the ingestion of food, or until actual contact of the 
arresting free hydrochloric acid with the ptyalin. 

Albumin 

Albumin is of the nature of globulin; it is precipitated by heat, 
and is found in very small amounts. The amount increases in 
Bright 's disease (Vulpian, Pouchet, Michaels). In one patient 
suffering from albuminuria of cardiac origin the percentage of 
albumin in the saliva was 0.145, and in one suffering from par- 
enchymatous nephritis it was 0.182 (Vulpian, with affirmative 
control by Pouchet). 7 

The Sulphocyanids (Potassium, Sodium and Ammonium) 
KCNS; NaCNS; NH 4 CNS 

Sulphocyanids are found in mixed saliva in proportions vary- 
ing from 0.0075 to 0.0100%. The proportion seems to be greater 
in individuals of the hyperacid diathesis than in those of the hy- 
poacid. Rheumatic patients exhibit a greater amount than gouty 
patients, but in patients with phosphaturia the amount is less 
than in gouty patients. The complete absence of sulphocyanids 
has been associated with gastrointestinal disorders. Prof. Gies' 8 
studies lead one to conclude that the amount of sulphocyanids 
in the saliva bear no relation lukatsoever to the incidence or prog- 
ress of caries. 



"Pickerill: Loc. cit. 

T Michaels, J. P. : Transactions of the Fourth International Dental Congress. 

journal of the Allied Dental Societies, 1911, vi, pp. 289, 297, 323, and 334. 



372 DENTAL PATHOLOGY 

Max Kahn likewise reports negative findings. 9 The sulphocy- 
anids in the saliva are products of protein metabolism and, 
Pickerill believes, of the breaking down of such mouth proteins 
as mucin, epithelium, leucocytes, etc. He adds that the sul- 
phocyanids in the saliva, "may have a beneficial effect, if only 
present in sufficient amount." This investigator found that the 
sulphocyanids could exert a slight antiseptic action if present in 
the saliva in a one per cent solution or over. But as the percentage 
is practically always constant and does not vary by the application 
of such stimuli as cause an increase in the percentage of other 
salivary constituents, the role of the sulphocyanids as a preventive 
of dental caries is nil. 

The amount of sulphocyanids may, however, be rapidly in- 
creased in man by the administration by mouth of repeated doses 
of potassium sulphocyanid of from % to 1 grain in water. The 
percentage in the saliva was increased to 0.0200 from 0.0100 (a 
fair average of sulphocyanid content) in three hours follow- 
ing a dose of 0.1 gram in water. This increased percentage per- 
sisted for seven days. 10 

Inorganic Constituents 

The inorganic salts are alkali and earthy phosphates, carbon- 
ates, bicarbonates and chlorides. The alkali group includes 
potassium and sodium phosphates; sodium carbonate and bicar- 
bonate (in fresh saliva); ammonium carbonate; potassium and 
sodium chloride. The earthy group includes calcium phosphate, 
carbonate, and bicarbonate, the latter in fresh specimens. Mag- 
nesium, because of its behavior toward analytic re-agents, is left 
in the so-called alkali group of metals (Simon). It is found in 
saliva as a phosphate and carbonate. The phosphates and car- 
bonates may exist in the saliva as acid or alkaline salts. 

In the gouty diathesis the proportion of chlorides is increased, 
and decreased in febrile affections. Ammonium carbonate is ac- 
cording to Michaels, a constant constituent of the saliva, being 
present in comparatively large proportions in the hyperacid diath- 
esis (rheumatism, gout). 



D Dental Cosmos, 1914, lvi, 175. 
10 Pickerill: Loc. cit. 



THE SALIVA 373 

In addition to all of the foregoing constant constituents of the 
saliva, Michaels records the pathologic presence of fatty phos- 
phorous compounds (lecithin and tyrosin), glycogen, biliary 
pigments and biliary acids 11 urobilin, cholesterin, glucose, so- 
dium and ammonium urates, urea, propionic acid, acetone, suc- 
cinic acid, etc. The presence of these abnormal constituents is 
associated with certain pathologic states. Thus, in the saliva of 
individuals of the hyperacid diathesis sodium and ammonium 
urates have been found; in salivas of diabetics, propionic acid, 
glucose, and acetone ; and in that of cholemics and uremics, bil- 
iary elements. 

Reaction 

The old time custom of testing the reaction of the saliva by 
means of litmus is utterly unreliable. The saliva exhibits an 
amphoteric reaction and as pointed out by Kirk, in a specimen of 
saliva the acidity is not due to an uncombined acid, but to the 
presence of a salt which has resulted from only the partial re- 
placement of the hydrogen by the metal; the alkalinity in the 
same specimen is due to the presence of the alkaline salt of the 
acid by replacement of twice the number of hydrogen atoms. 
Thus, in a specimen of saliva the presence of the acid ion of the 
basic salt of phosphoric acid may cause blue litmus to turn red 
and the basic ion may cause red litmus to turn blue, if the salts 
do not neutralize each other. 

Phenolphthalein is the indicator most commonly employed. 
The Scientific Research Committee of the National Dental As- 
sociation has recommended that it be used as an indicator and 
titration be made against NaOH. Phenolphthalein is, however, 
sensitive to C0 2 , which may obscure the reaction for free and 
uncombined acids. Bunting 12 recommends the passing of C0 2 - 
free air through the sample to be tested, while heated to a tem- 
perature not over 50° C. All uncombined C0 2 will be discharged 
in from five to ten minutes. This method is less objectionable 
than that of boiling the saliva. Saliva, the mixed secretion of the 
parotid, submaxillary, sublingual, and buccal glands is alkaline to 
litmus although the same specimen may be amphoteric to litmus 



"Gorup-Besanez: (Quoted by Michaels, J. P., loc. cit.) 

12 Bunting: Official Bulletin of the National Dental Assn., October, 1914, i, Xo. 4, 
p. 38. 



374 DENTAL PATHOLOGY 

owing to the presence of acid and basic phosphates and carbon- 
ates. Saliva is as a rule acid to phenolphthalein because of the 
presence of C0 2 and acid phosphates and carbonates; it usually 
is alkaline to methyl orange, which is not affected by C0 2 . All 
salivas are hence alkaline to the latter indicator and to lacmoid 
and Congo red. The amphoteric behavior of the saliva is due to 
the presence in the fluid of free H and OH-ions and the reaction 
of the fluid is determined by the predominance of either of these 
groups of free ions. The saliva from a resting gland differs in 
reaction from that flowing under a stimulus, 13 and as shown by 
Pickerill the reaction varies according to the nature of the stimu- 
lus and the length of time it is applied. The result of this stimu- 
lation differs in different individuals. Thus it has been found 
by this investigator that the alkalinity is increased by acid 
stimuli which, from among all other substances, produce the 
greatest alkalinity per cubic centimeter, and that the alkalinity 
is depressed by such articles of daily food as white and brown 
bread, with or without butter, and cake, biscuit, meat and sweets. 
Pain causes a very alkaline reaction. The average alkalinity of 
the parotid saliva per cubic centimeter is greater than that from 
the other glands; but as the rate of flow from this gland is low, 
the total alkalinity per minute is very much less (Pickerill). 

The character and the amount of normal or abnormal constit- 
uents of the saliva reflect to quite an extent the nature of the 
biochemical reactions in the body. It varies in composition not 
only in different individuals, but at different times in the same 
individual, because of the temporary or constant results of 
nutritional phenomena and of bacterial or chemical intoxications. 
The investigations of Michaels, Gies, Kirk, Pickerill, Howe, Bunt- 
ing, Ferris and others have made it possible to enlarge our knowl- 
edge of saliva and of its possibilities in semeiology. Howe, for 
instance, has shown that an excessive carbohydrate diet is mani- 
fested in the saliva by the presence of imperfectly oxidized 
bodies ; that in artificially induced glycosuria the saliva contains 
traces of glucose or an aldehyde, and, in intestinal disturbances, 
traces of indican. Howe's investigations have led to conclusions 
confirmatory of the work of Michaels and Kirk: that the saliva 
is a fair barometer of normal and abnormal body reactions. 



"Howe, Percy R. : Dental Cosmos, lv, 1913. 



CHAPTER XXVI 

THE GUMS AND GINGIVAE 

Normal and Pathologic Considerations 

The gums are the soft tissues which cover the alveolar process 
of the maxilla and mandible and extend from the crest of the 
alveolar process to the commissure of the lips and cheeks exter- 
nally; and internally are continued, in the maxilla with the pala- 
tal mucous membrane, and in the mandible with the mucous mem- 
brane of the floor of the mouth. 

The gums consist of an underlying fibrous connective-tissue 
mat containing a few elastic fibers, and of an external covering of 
stratified squamous epithelium (Figs. 292, 293, and 294). The 
underlying fibrous connective-tissue mat, designated as the tunica 
propria or the stroma of the mucous membrane, presents a number 
of elevations, or papillcv, which penetrate into the epithelial layer, 
giving to the oral mucous membrane an appearance under the mi- 
croscope sui generis. Connective-tissue cells, round, stellate and 
spindle-shaped, are supported by the fibrous tissue of the tunica 
propria. The mucous membrane is connected with the underlying 
structure by means of a layer of areolar tissue, i.e., the submucous 
layer. The attachment of the mucous membrane may, under 
normal conditions, be very firm as in the case of the gums and the 
mucous membrane covering the hard palate, or very loose, as in 
the case of the buccal and labial mucous membrane and that form- 
ing the lining of the floor of the mouth. The blood supply of the 
gums is very rich, being distributed to the connective-tissue under- 
structure (stroma) the epithelial covering obtaining its nutrition 
by osmosis from the capillary loops at the apices of the papilla?. 
The arteries after penetrating and passing through the submucous 
areolar tissue, break up into arterioles, which in turn break up 
into capillary loops in the substance of the papillaa in close rela- 
tion with the epithelial layer. The veins follow the arteries in 
their general course. The nerve supply is good, but the gums are 
not, when normal, as sensitive to pain as other mucous mem- 
branes, and particularly is the sensitiveness reduced in the pos- 

375 



376 



DENTAL PATHOLOGY 



terior, or lingual, portion of the gum due, undoubtedly, to the con- 
stant traumatism it is subjected to in the process of mastication. 

GINGIVAE 

Normal and Pathologic Considerations 

By the term gingiva is meant that extension of the gum tissue 
proper which, starting at the crest of the alveolar process, reaches 




Fig. 292. — Normal gingiva of sheep. The relation of its cellular elements is similar 
to that in the human structures. The cells being larger, the tissue can be studied more 
satisfactorily than in the human specimen. In man, the horny layer, (stratum corneum) 
is not nearly as prominent as it appears in this specimen, a, area in which individual 
epithelial cells with t heir respective nuclei can be clearly seen; b, stratum germinativum 
or stratum Malpigliii; c, connective tissue stroma; d, capillaries in connective-tissue 
papilla. (Section by Dr. A. C. La Touche.) 

to the free unattached margin of the gingivae, called the gingival 
border. It is composed of (1) the body of the gingivae, or that 
portion which is attached, 1 at one end, to the crest of the alveolar 
process by means of the fibers of the alveolar periosteum, and 



*G. V. Black's classification. 



THE GUMS AND GINGIVA 



377 



at the other to that portion of the root between the alveolar 
crest and the cementoenamel junction by means of the fibers of 
the peridental membrane; of (2) the free gingiva?, or that un- 
attached portion of tissue which extends on the labial, buccal and 
lingual surfaces for a distance of from one to five millimeters; 
and of (3) the septal gingivae, or that portion of tissue which 




W IE MtuJfmm 




Fig. 293. — Gingiva of sheep. The arrangement of the epithelial and connective tis- 
sue structures is identical to that found in man. At the gingival cul-de-sac (subgingival 
fold) in man the epithelial layer becomes thinner, affording little protection against in- 
fectious agents which upon breaking through the epithelium involve the underlying con- 
nective tissue mat from whence the possibility of metastasis is self-evident, a, stratum 
corneum, or horny layer; b, b, stratum germinativum or stratum Malpighii; c, c, capil- 
lary network in papillss from underlying connective-tissue stroma (mat) ; d, d, connec- 
tive-tissue stroma; c, blood vessel in stroma; /, epithelium lining internal surface of gingi- 
val cul-de-sac, g. 

almost entirely fills up the interproximal space to a short dis- 
tance from the contact point, and which springs from the ap- 
proximal portions of the body of the gingiva?. 

To the gingivae are attached sets of fibers from the peridental 
membrane as follows : 



378 



DENTAL PATHOLOGY 



A group of fibers which springs from the peridental membrane 
and is attached to the body of the gingivae; a group of fibers 
which runs a little below the alveolar crest and connect the peri- 
dental membrane of one tooth with that of another. This group 
of fibers passes through the septal gingivae. A group of fibers 
runs from the peridental membrane, curving at first in an oc- 
clusal direction and then becomes attached to the crest of the al- 
veolar process. 




Fig. 294. — Human gingiva. The dark border, a, a, is the stratified squamous epithelial 
lining. Between the epithelial prolongations and within the eonnective-tissue papillae are 

found the capillary loops at b; the connective tissue stroma at c, is composed of connective 
tissue fibers and of round, stellate, and spindle-shaped cells. The epithelial layer being 
devoid of blood vessels its nourishment is derived by osmosis from the capillary loops in 
the connective tissue papilla. 



Functions 

The functions of the gingivae are protective so far as the peri- 
dental membrane is concerned. They encircle the tooth in its 
entirety from the alveolar crest to the external or free gingival 
border over a distance of several millimeters. The consistence 
and contour of the gingivae favor the gliding of food over their 
surfaces in the course of mastication, with the minimum of lodg- 
ment of debris against the free border, and this protection is 
further augmented by the crown contour commonly described 



THE GUMS AND GINGIVAE 379 

as bell-shaped. 1 This arrangement exists when the tissue 
is not subjected to abnormal degrees of mechanical, chemical, or 
other forms of irritation. The septal tissues depend to a large 
extent upon the character of the contact point for the mainte- 
nance of their physiologic function. Lack of contact or broad 
contact, between two approximal surfaces leads in time to dis- 
ease of the gingiva?, and ultimately to involvement of the periden- 
tal membrane and alveolar process. 

Black and Noyes attach considerable importance to the gin- 
givae in maintaining the correct relationship of the teeth to each 
other and to the arches. They argue that following the extrac- 
tion of a tooth a mass of cicatricial tissue is formed at the point 
where the transseptal fibers are attached, (i. e.. the peridental 
fibers which cross from the peridental membrane of one tooth to 
that of another), and that the contraction of this tissue moves the 
adjacent teeth bodily toward one another. It is unquestionable 
that disease and destruction of the gingivae bring about mal- 
position of the teeth, as frequently seen in pyorrhea alveolaris, 
where a tooth will move in a direction away from the so-called 
pus pocket. This is due to the fact that the peridental fibers on 
the affected side have been lost or destroyed, the pull of the 
group of fibers on the opposite tooth surface carries the tooth away 
from the area of peridental and gingival involvement. Destruc- 
tion of the group of fibers which attaches to the crest of the alveolar 
process results in the extrusion of the tooth, a phenomenon observ- 
able in pyorrhea alveolaris. 

The epithelium which covers the gingiva' exercises under nor- 
mal conditions, a protective function similar to that which per- 
tains to the epithelium of the covering of the body. In the 
case of the free and septal gingivae the epithelium covers its ex- 
ternal surface as well as the subgingival space (i. e., that sur- 
face in contact with the enamel at the neck of the tooth), al- 
though upon the internal aspect the stratum corneum (horny 
layer) is attenuated or absent. In people who are careless in the 
hygiene of the mouth, food debris and mucin become lodged 
against the free border of the gingivae and there undergo de- 
composition, with the formation of acid or alkaline end products. 
The gingivae are thus at first merely irritated; but by unclergo- 



iFriesell, H. E. : Jour. National Dental Assn., vi, 579. 



380 DENTAL PATHOLOGY 

ing a decrease in their power of resistance by reason of this con- 
stant irritation, they soon become the seat of bacterial activity. 
Degeneration and death of the epithelial cells lining the gingivse, 
particularly of those lining the subgingival space, follow, and 
these tissues and the underlying connective-tissue stroma become 
not only the seat of bacterial activity, but also an active source 
of absorption for bacteria and their toxins. It is well to remem- 
ber that the papillae of the tunica propria contain capillary loops 
and that perivascular lymph spaces are also present. Absorption 
of these noxious substances occurs by the hematogenic or lympho- 
genic routes, or by both. Clinically the writer has observed and 
studied a large number of patients exhibiting symptoms of gen- 
eral toxemia and of infection in the digestive and respiratory 
organs, which improved markedly by proper treatment being 
directed at these tissues ; viz., the subgingival spaces. While the 
life and usefulness of the peridental membrane depend to such a 
large extent upon the health and integrity of the gingival tissues, 
again the latter depend for their OAvn health and physiologic ef- 
ficiency upon the topography of the teeth and the character of 
the contact between the approximal surfaces.* 



*Hartzell in his investigation of gingival infections and subsequent systemic involve- 
ments has thrown considerable light on the absence of protectiveness in the subgingival 
cul-de-sac. The reader is referred to his writings in the files of the Journal of the 
National Dental Association. 



CHAPTER XXVII 

CALCAREOUS DEPOSITS 

Calcareous deposits upon the surfaces of teeth are divided, from 
the standpoint of their origin, into salivary and subgingival (se- 
rumal and sanguinary). The former originate entirely from the 
saliva, the latter probably partly from the saliva and partly from 
sources other than the saliva, viz., blcod, lymph, and pus. Cal- 
careous deposits throughout the body, including, of course, de- 
posits upon the crowns and roots of teeth, are invariably composed 
of an or ganic matrix which becomes impregnated with inorganic 
salts. The organic nucleus, or matrix, is the binding substance. 
In the mouth the organic matrix is a mixture of mucin, epithelial 
cells, food debris, and bacteria. In the duets of the salivary glands 
the calcareous deposit, when present, is composed of an organic 
matrix made up of a thickened secretion of the epithelial lining 
of the duct. 1 

Calcareous masses in the intestines are formed by the deposition 
of calcium phosphate, calcium carbonate and ammonio-magnesmm 
phosphate, in varying proportions: arterioliths (calcareous depos- 
its in the arteries), and plileboliths (calcareous masses in the 
veins), are clue to the calcification of thrombi. It will therefore be 
seen that the general arrangement of the calculus is fundamentally 
identical, no matter where found. 

Two theories have been advanced in explanation of the phenom- 
enon of salivary calculi (tartaiO formation. One of these worked 
out by the late H. H. Burchard is based upon the theory that the 
solubility of water for certain salts of calcium is increased when 
the water holds carbon dioxide in solution, so that, upon the escape 
of any carbon dioxide from solution, any amount of soluble cal- 
cium salts previously held in solution above the normal amount 
which the water can hold, will be precipitated. He argues that 
the saliva, after it is poured into the mouth, loses its carbon dioxide 
contents, and that calcium salts, particularly calcium phosphate, 
are precipitated upon and into a mass of organic debris composed 



'Ziegler: General Pathology, New York, Wm. Wood & Co. 

381 



382 DENTAL PATHOLOGY 

of mucin shreds, epithelial cells, food debris and bacteria. That 
the end product of carbohydrate fermentation constantly going on 
in the mouth, especially in locations in which food debris is re- 
tained because of inaccessibility to the toothbrush or to muscle 
and tongue action, furnishes a sufficient amount of acid to pre- 
cipitate the mucin; and that this precipitate, together with 
bacteria and desquamated cells, forms the organic nucleus which 
becomes impregnated with calcareous salts. 

Clinical examinations show that these deposits are found upon 
surfaces in proximity to the openings of the ducts of the salivary 
glands, namely, the buccal surfaces of the upper molars and the 
lingual surfaces of the lower central and lateral incisors. These 
deposits occur upon surfaces which are rough. Congenital or ac- 
quired enamel defects are to be constantly borne in mind in con- 
nection with the study of the prophylaxis of calcareous deposits. 
A tooth surface that is smooth and polished does not favor deposits of 
tartar. Also, surfaces which are constantly subjected to friction 
in the course of mastication by the tongue, cheeks or lips are, as 
a general rule, free from deposits. Concerning the nature of tar- 
tar composition Kirk 2 analyzes the studies of Rainey, Harting, 
and of Ord, explaining that when certain earthy salts are pre- 
cipitated in a medium containing a colloidal substance in solu- 
tion the resulting precipitate, instead of being crystalline, is in 
the form of minute spheroidal masses; and further, that as the 
precipitation progresses, these spheroidal masses increase in 
diameter so that adjoining masses grow into contact, and by 
accretion of new material these spheroidal masses coalesce, giv- 
ing rise to mulberry-like bodies. 

Professor Harting 3 extended his experiments and showed that 
when the precipitates are formed in egg albumen, blood serum, 
or a solution of gelatin, a variety of forms may be produced 
which resemble concretions found in the animal body. The 
basic substance or matrix which results after deposition, if treated 
with an acid, dissolves out the inorganic constituents of the con- 
cretion, and he named the residue calco-globulin. The spheroidal 
bodies he named calco-globulin. 

As has already been shown, the mixed saliva contains a propor- 



2 Kirk: American Textbook of Operative Dentistry, Philadelphia, Lea & Febiger. 
3 Ibid. 



CALCAREOUS DEPOSITS 



383 



tion of calcium salts in solution, most of which is calcium phos- 
phate; and consequently the main inorganic ingredient of salivary 
deposits is calcium phosphate. Unmixed parotid saliva deposits 
calcium carbonate on standing. Kirk is of the opinion that as a 
result of putrefactive decomposition in the mouth, ammonia is 
formed, and that the ammonia will precipitate calcium phosphate 
from its acid solution as calcium ammonium phosphate, or, when 
magnesium phosphate is present in addition to calcium phos- 
phate, also as ammonium magnesium phosphate, a salt which 
is found to be one of the constituents of certain forms of tartar. 
A form of deposit caused by the chewing of the betel nut is 
of rapid formation and extremely destructive to the investing 
tissues. 




Fig. 295. — Salivary calculi on the lingual surfaces of the roots of lower cuspids. The 
proximity of these surfaces to the mouths of the ducts of the submaxillary and sub- 
lingual glands is the reason for their vulnerability to these deposits. 



In essence, the theory just outlined is one which assumes that 
the organic nucleus of the salivary deposits is furnished by 
precipitated mucin, desquamated epithelial cells, food debris, 
bacteria, etc., as found in the mouth ; and that the inorganic ma- 
terial is furnished by the saliva which, as it pours into the mouth, 
loses to a certain extent its holding power for a number of inor- 
ganic salts, particularly tricalcium phosphate (Ca 3 (POJ 2 ). G. 
V. Black, on the other hand, believed that calcareous deposits 
upon the surfaces of teeth, either salivary or subgingival, are 
formed by the deposition upon slightly roughened surfaces of 
teeth, of a combination of an organic material (possibly a globulin 



384 



DENTAL PATHOLOGY 



which he named agglutinin of salivary calculus) with inorganic 
salts. In this theory it is assumed that the organic and inorganic 





Fig. 296. — Voluminous salivary calcu- 
lus with shelf-like formation which rested 
upon the mucous membrane of the floor 
of the mouth. 



Fig. 297. — Salivary calculus with shelf- 
iike formation. 





Fig. 298. — Salivary calculus in lower 
right incisor which had accumulated to 
within one-eighth of an inch of the apex. 
Observe the saddle-like arrangement of 
the deposit on the lingual aspect, resting 
upon the soft tissues. 



Fig. 299. — Salivary calculus which had 
attained considerable size and had caused 
the exfoliation of the tooth. The apical 
area was entirely covered by the deposit. 



elements of salivary calculi are brought together into the mouth 
in the saliva and deposited upon the surfaces most accessible to 



CALCAREOUS DEPOSITS 



385 




Fig. 300. — Salivary cal- 
culus in lower incisor 
which had caused the ex- 
foliation of the tooth. 



Fig. 301.— Salivary cal- 
culus covering all of the 
crown and most of the root 
of the tooth. 



Fig. 302. — Salivary cal- 
culus which covered a large 
area of crown surface and 
all of one-half the root sur- 
face, the latter upon all as- 
pects. 




Fig. 303. — Salivary calculus 
on lower right cuspid involving 
approximately two-thirds of the 
root. 



Fig. 
calculus 
pect of 



304. — Salivary 
on lingual as- 
the root of a 



lower central incisor. 



Fig. 305. — Salivary 

calculus covering a por- 
tion of the labial surface 
of a lower right centra! 
incisor and reaching on 
the disto-lingual aspect 
over one-half the length 
of the root. The invest- 
ing tissue had been de- 
stroyed to a level slightly 
beyond the lowest edge 
of the calculus. 



386 



DENTAL PATHOLOGY 



the ducts of the salivary glands. He found that the deposit will 
form in preference upon surfaces of teeth which have lost their 
natural smoothness or polish, and also that while the quality of 
the ingested food played a small part in the production of calculi 
the same could not be said of the quantity. 

Salivary deposits vary from the minutest possible particle to 
such a size as to cover the roots of several teeth from the gin- 
gival margins to the apex (Figs. 295-309). They do not occur 
in every mouth. Some individuals are practically free from them, 
while with others they form rapidly in spite of careful brushing 
of the teeth. They vary in color from a very light chalky color 





Fig. 306. — Salivary calculus entirely Fig. 307. — Voluminous salivary deposits 

covering the buccal surface of the crown upon buccal and part of the occlusal sur- 

and onedialf the length of the roots of an faces of an upper molar, 
upper left first molar. 



to a deep yellow. The yellowish variety is usually the harder. There 
is a gradual increase in density from the time of the first deposi- 
tion until the calculus assumes a decidedly hard texture. During 
the beginning of their formation, varying in different individuals 
from a few days to a few weeks, they are soft and may be re- 
moved by a thorough brushing of the teeth. In contact with the 
gingivae as they invariably are, they produce degrees of irritation 
which lessen the power of the tissues to ward off infection, at 
the same time rendering the field a favorable one for bacterial 
activity. 



CALCAREOUS DEPOSITS 



387 



Lesions in the Investing Tissues Caused by Salivary Calculi 

The deposition begins at the gingival margin, and, following a 
decrease in the resistance of the soft tissues by virtue of the me- 
chanical irritation induced by the deposit, bacteria invade the 
area. An inflammation follows which results eventually in a 




Fig. 308. — Large masses of salivary calculi removed from the teeth to which they wei 

attached. 




Fig. 309. — Large masses of salivary calculi. 



destruction of those peridental fibers which are attached to the 
gingiva, with a loss of structure in the alveolar process and over- 
lying gum tissues. The disappearance of the alveolar process, 
as well as of the gingival tissue, is the result of an absorption 
of these structures consequent upon nutritional interference, but 
may also be the result of the liquefaction of tissue cells incident 



388 DENTAL PATHOLOGY 

to bacterial activity in the part; or it may be the result of both. 
The deposit is at first located upon the enamel at the gingival 
margin, but as destruction of the peridental fibers occurs 
and the alveolar process and the gum tissue gradually disappear, 
if the deposit be not removed it will increase in size and again 
impinge upon the peridental fibers, so that the noAV receded 
alveolar process and gingival tissue will again suffer another 
series of pathologic phenomena similar to that just described. 
In this way the process goes on unless the deposit is removed 
by instrumental means. The type of inflammation which these 
salivary deposits induce in the investing tissues should be clearly 
differentiated from the disturbances induced by other forms of 
calcareous deposits. In the case of the salivary variety, the 
destruction of the investing tissue reaches but a short distance 
beyond the deposit, and when the teeth are thoroughly scaled and 
polished, and the gum tissue property stimulated by suitable 
medication, a return to a healthy condition is invariably the case. 
The gum tissue can not, however, be brought back to its original 
relation with the gingival margin. The denuding of the ce- 
mentum will be permanently established. Attempts have been 
made in the past to remedy gum recession by surgical means, but 
the results have not so far justified the means. 

P. Rosenthal 4 recommends the following teclmic to remedy 
recession* -.of the gums — the result of deposition of tartar, trau- 
matism. -erosion, or caries. He calls attention to the necessity of 
first restoring the surface contour of the tooth, if necessary, by 
gold fillings. 

"The gum above the tooth to be operated on is carefully ster- 
ilized with tincture of iodin, and a horizontal incision is made 
the width of the tooth, at right angles with the long axis and 
sufficiently high up on the gum to furnish a good-sized flap. This 
incision should involve the periosteum. The flap is then stripped 
off the bone by inserting a fine instrument under it, starting at 
the neck of the tooth, and should be large enough to allow of easy 
mobility. A silk ligature is then passed under the central por- 
tion of the flap parallel with the incision and taking in almost 
the entire breadth of the flap. Another ligature is tied tightly 
around the free portion of the tooth, and to this ligature the first 
ligature is secured, the flap being drawn up a little higher than 

4 Le Laboratoire, Paris, November 26, 1911, Dental Cosmos. 



CALCAREOUS DEPOSITS 389 

the normal gum line of the tooth to allow for a recession from 
cicatrization. The wound and the ligature are painted with 
tincture of ioclin, this antiseptic treatment to be repeated daily. 
From the second day on the gum is massaged in the direction of 
the long axis and toward the free portion of the tooth. On the 
fifth or sixth day the ligatures are removed. As a rule, cicatriza- 
tion is then sufficiently advanced to prevent recession of the flap. 
The primary incision would fill up completely without leaving a 
scar. Eosenthal claims that in cases kept under observation for 
several years the results are still perfect. 

In summarizing the effects of salivary deposits upon the in- 
vesting tissues, it must be stated that salivary deposits exercise 
a detrimental influence by reason of 

1. Mechanical irritation of the gingiva and peridental mem- 
brane. 

2. By favoring the deposition and decomposition of food par- 
ticles, either fermentation or putrefaction, or both. 

3. By rendering the field of their location a suitable one for 
bacterial invasion — lowered vital resistance. 

The products of these processes of molecular simplification — 
fermentation or putrefaction of food particles — produce a degree 
of irritation in the investing tissues which invites bacterial in- 
vasion. Bacteria play a leading part in the process. 

The form of disturbance caused by salivary deposits — salivary 
calculi gingivitis — may be localized or generalized throughout the 
mouth. In the former case the investing tissues over one or a 
few teeth only are affected; in the latter case the investing tis- 
sues throughout the mouth are affected. The clinical symptoms 
of salivary calculi gingivitis are: 

1. Disappearance of the gingiva and gums as the result of 
pathologic absorption (atrophy), bacterial activity, or both. 

2. Congestion and tumefaction of the gingiva and gums. 

3. Bleeding at the slightest provocation. 

4. A change in the color of the tissues from a healthy pink to 
a deep red, purple, or bluish black. 

5. Putrefactive and fermentative changes. 

6. Tenderness or pain upon mastication, or upon the intro- 
duction of irritating articles of food. 

7. Fetor of breath. 

8. Systemic involvement. 



CHAPTER XXVIII 

SUBGINGIVAL DEPOSITS 

Etiology 

Subgingival deposits are those which are in the first place 
formed under the free gingiva. They are of a darker color than 
the salivary deposits and are also harder. The darker the de- 
posit, the more adherent it is to the root. They are evidently 





Fig. 310. — An upper lat- Fig. 311. — Subgingival Fig. 312. — Subgingival 
eral incisor with its root depo.sits in upper right lat- deposits in upper right dis- 
covered with subgingival cral incisor, distal view. pid. 
deposits over half of its 
length. 

the result of an abnormal degree of irritation of the gingival 
tissues (Pigs. 310-316). The irritation is afforded by the de- 
composition of food debris and mucin at the necks of the teeth, 
by ragged or rough edges of fillings, poorly adapted gold crowns, 
or from any other form of prosthetic appliance or defective res- 
toration leaving a rough edge at the neck of the tooth which 
continually irritates the gingiva. Any form of injury to the gin- 
giva may become the etiologic factor in the deposition of subgin- 

390 



SUBGINGIVAL DEPOSITS 391 

gival deposits. Gingival irritation is not, however, by any means 
entirely due to defective crowns or fillings, but may be brought 
about by defective or insufficient contact points leading to food 
impactions in the interproximal spaces, with concomitant irri- 





Fig 313.— Subgingival deposits in *«?• . 314.— Subgingival deposit, in 

upper right second molar. "PP>t right second molar.. These de- 

11 • - posits were greenish in color and sur- 

rounded the tooth at the enamel;ce- 
mentum junction upon all of its 
faces except the lingual. 





Fig. 315. — Roots of a molar cov- Fig. 316. — Subgingival deposits on 

ered with subgingival deposits. the anterior and posterior roots of a 



tation of the gingivae ; they likewise may be induced by the pres- 
ence of salivary calculi. Salivary and subgingival deposits may 
be found upon the same tooth, the supposition being that the 



392 DENTAL PATHOLOGY 

salivary deposit was formed first and the other occurred fol- 
lowing the gingival irritation induced by the former. It is not 
infrequent that patients have their teeth scaled and polished 
and consequently have the salivary deposits entirely removed, 
while the subgingival deposits remain untouched. In this way 
we may in part account for the fact that in a number of in- 
stances the subgingival deposit is found while the salivary is not 
to be seen. 

The subgingival deposit, once formed, irritates the gingiva, 
thereby inviting bacterial activity. As the result of the infection, 
the peridental fibers are destroyed so that additional deposits 
of calculi will form and encroach upon the still attached border 
of the peridental membrane. Infection will become active again 
and more peridental fibers will be destroyed, the process ad- 
vancing in this way until a so-called "pocket" results. This proc- 
ess of pocket formation is decidedly chronic in the sense that 
it is of slow formation, years elapsing in most cases before a 
well-formed pocket is present. It is not to be assumed, how- 
ever, that in the presence of any one or several of these etiologic 
factors, subgingival deposits will be invariably present. The 
inorganic salts in suitable amount must be present in the gin- 
gival exudate and the conditions leading to the formation of the 
organic matrix must be present, and then this takes place only 
when the body metabolism is disturbed, even though only slightly. 

LESIONS PRODUCED BY SUBGINGIVAL DEPOSITS: 
CHRONIC GINGIVITIS 

Pathologic Anatomy 

The student should bear in mind the striking difference in the 
character of the effect upon the investing tissues of salivary de- 
posits and of subgingival deposits as originally pointed out by 
G. V. Black. In the former, well-defined pus pockets are rare, 
while in the latter form pockets almost invariably follow. The 
early deposition of subgingival calculi can be detected by the 
color of the gingiva?, which are of a deep red, in some instances 
running to a blue, purple, or even black. The tissues are flabby 
and present an appearance typical of a chronic inflammation. 
The stratified squamous epithelium dips into the connective tis- 



SUBGINGIVAL DEPOSITS 



393 



sue to a greater length than is the case with normal epithelium, 
and the connective-tissue mat of the mucous membrane is almost 
everywhere infiltrated with large masses of round cells, most of 
which are mononuclear leucocytes, large and small, plasma cells, 
lymphocytes and polymorphonuclear leucocytes in small numbers 
(Figs. 317, 318 and 319). Mast cells so often found in 
mucous membranes which are the seat of chronic inflammation 



a \mk 




Fig. 317. — Section of human gingiva. The stratified squamous epithelium has lost 
its characteristic appearance; the projections of epithelial cells between the papilla; of 
connective tissue have become elongated. The gingiva was the seat of a chronic inflam- 
mation which by continuity involves the peridental membrane and the alveolar process. 
It marks the beginning of pocket formation. a, a, elongated epithelial projections; b, 
connective-tissue stroma. 



are also to be seen. The infection spreads slowly as a general 
rule, and, involving the fibers of the peridental membrane and the 
alveolar process, initiates the progressive process of destruction 
in the supporting tissues of the tooth (Figs. 320-325). The pus 



394 



DENTAL PATHOLOGY 



pocket is the result of the destruction of the peridental fibers 
and of the alveolar process. The proteolytic toxins formed in 
the course of the inflammatory process liquefy the peridental 
fibers. 

The pathologic phenomena which develop in the bone of the 
alveolar process in pocket formation are characteristic of an 




Fig. 318. — Chronic inflammation of gingiva. The epithelial prolongations in the sub- 
jacent connective tissue elongate as the result of the continued low degree of irritation. 
The connective-tissue stroma has lost its characteristic appearance and the cells and fibers 
which were present under normal conditions have been replaced by inflammatory cells; 
i. e., mononuclear wandering cells comprising mononuclear leucocytes, lymphocytes, and 
plasma cells and polymorphonuclear leucocytes in small numbers, a, a, elongated epithelial 
projections; b, b, round cell infiltration. Mast cells are also to be located under the 
higher magnifications. 



infectious osteomyelitis. The medullary substance contained in 
the cancellated spaces becomes the seat of a chronic inflamma- 
tion in which osteoclasts play an active part. The hard sub- 
stance of the bone disappears through osteoclastic action, the 



SUBGINGIVAL DEPOSITS 



395 



cancellated spaces are eaten through, and the Haversian canals 
widened. The contents of the spaces become filled with large 
masses of inflammatory cells, viz., mononuclear and polymorpho- 
nuclear leucocytes, lymphocytes, plasma cells, and giant cells. Suc- 
cessively the bone lamella? are destroyed or carried away by osteo- 
clasts and the inflamed medullary contents of the canal breaks down. 




Fig. 319. — Chronic inflammation of the free gingiva. The tissue has lost all its 
histologic characteristics and is gradually disappearing as the result of interference with its 
nutrition, and cell liquefaction. 

Kirk 1 believes that "the principles governing the precipitation 
of earthy phosphates and carbonates directly from the saliva 
in the production of true salivary tartar govern also the pro- 
duction of the girdle-like concretions that are found encircling 
the teeth at and below the anatomic neck and beneath the gum 



iRirk: American Text-book of Operative Dentistry, Philadelphia, Lea & Febiger. 



396 



DENTAL PATHOLOGY 



margin." The preliminary step in the formation of subgingival 
deposit this investigator attributes to the retention under the 
gingival tissues of an inflammatory exudate rich in colloid ma- 
terial, the latter being the binding material of the deposit, giv- 
ing to it its characteristic hardness. The difference in color be- 




W f 




Fig. 320. — Gingivitis, chronic, advanced stage, the infection is progressing toward the 
peridental membrane, a, dentin; b, cementnm; c, c, stratified squamous epithelium lining 
subgingival space; d, d, fibers of peridental membrane in the gingiva; e, e, round cell in- 
filtration. 



tween salivary and subgingival deposits is believed to be due 
to the formation of sulphomethemoglobin; the source of the 
hemoglobin is from the disintegration of erythrocytes, and the 
sulphur from the putrefactive changes in nitrogenous food re- 
tained at the gingival margin. 



SUBGINGIVAL DEPOSITS 



397 



In sections of the gingivae the layer of stratified squamous epi- 
thelium and the epithelial prolongations into the underlying connec- 
tive tissue assume unusual forms by reason of a pronounced pro- 
liferation of epithelial cells and also on account of the level at 
which the section is cut. In the interpretation of sections of a 
gingiva which has been the seat of a chronic infectious process, these 
facts should be borne in mind. 




Fig. 321. — Gingivitis, chronic, advanced stage, induced by subgingival deposits, a, 
subgingival cul-de-sac; b, b, portions of stratified squamous epithelium from the internal 
lining of the gingival cul-de-sac; c, break in the epithelial layer marking one of the 
portals of the infection (the bit of tissue projecting out was torn in mounting the section); 
d, d, round-cell infiltration; c, fibers in the connective-tissue stroma. 






398 



DENTAL PATHOLOGY 




.J> 



Fig. 322. — Progressive chronic gingivitis. Decalcified longitudinal section. The in- 
fection which originated at the gingival margin has advanced to where the peridental 
membrane begins. It is only a matter of time befote the peridental fibers which are 
attached to the crest of the alveolar process will become involved, a, alveolar septum; 
b, crest of alveolar process; c, peridental fibers which are attached to the crest of the 
alveolar process; d, dentin; c and f, areas of round-cell infiltration marking the progress 
of the infection. 






SUBGINGIVAL DEPOSITS 



399 




Fig. 323. — Chronic inflammation of gingiva. The light area at the lower section of the 
picture is the subgingival cul-de-sac. To the left of the picture a portion of cementum 
and dentin is to be seen, while to the right of the picture is the gingiva and gum. a, 
subgingival space; b, dentin; c, cementum; d, epithelium of subgingival space; e, point 
at which infection has brought about liquefaction of epithelial lining; f,f,f, areas of 
round-cell infiltration. (Chronic inflammation.) 



400 



DENTAL PATHOLOGY 

b 




Fig. 324. — Chronic inflammation in the gingiva which has spread to the peridental 
membrane. An area of marked chronic involvement (round-cell infiltration) is seen 
in the horizontal peridental fibers, a, a, alveolar process; b, b, cementum; d, d, horizon- 
tal fibers of the peridental membrane; e, an area of involvement which includes some of 
the horizontal fibers of the peridental membrane. 



SUBGINGIVAL DEPOSITS 



401 




Fig. 325.— Progressive chronic gingivitis, a. cementum; b, space produced by detach- 
ment of cementum from dentin in process of decalcification and sectioning; d, fibers 
running from peridental membrane into gingiva; e, f, and g, stratified squamous epithe- 
lium lining internal surface of gingival cul-de-sac; h and i, round-cell infiltration in 
gingiva (chronic inflammation) progressing in the direction of the fibers of the peri- 
dental membrane at / and d. 



CHAPTER XXIX 

DISEASES OF THE PERIDENTAL MEMBRANE 

The peridental membrane, 1 or pericementum (alveole-dental peri- 
osteum, or root membrane) is a fibrous structure with a rich vas- 
cular and nerve supply, devoid of elastic fibers, encircling the 
root of the tooth in its entirety, and attached to the cementum 
by means of fibers which bear the same relation to the cementum 
as the periosteal fibers of Sharpey do to bone (Figs. 326, 327 and 
328). 

The functions of the peridental membrane are: 

1. To act as the means of attachment of the tooth to the al- 
veolus. 

2. To exercise a cushion-like function, thereby protecting the 
more sensitive internal organ of the tooth, i.e., the pulp, from 
traumatism such as would result from mastication, blows, etc. 

3. To act as a nourishing periosteum to the cementum and as 
the source of collateral circulation to the alveolus. 

4. To maintain the gingival contour by virtue of the arrange- 
ment of its fibers at the neck of the tooth. 

5. To absorb and build alveolar bone and cementum during the 
life of the tooth in response to degrees of stimulation, and until 
such time as occlusion has been permanently established. 

6. Tactile function. 

It is thicker near the neck of the tooth and in the apical re- 
gion, but becomes thinner throughout with age. This fact ac- 
counts for the greater susceptibility of the peridental membrane 
to infectious processes in the middle-aged and the old. "With a 
thinning of the membrane there occurs a decrease in the num- 
ber and in the caliber of arteries and capillaries, and the less- 
ened circulation in the membrane renders more difficult or im- 
possible the warding off of infectious processes. 

The blood supply of the pulp and that of the peridental mem- 
brane are intimately associated. This consists of a variable num- 



1 We are indebted to the late Dr. G. V. Black and to Dr. F. 13. Noyes for their 
valuable investigations of the histologic elements of the peridental membrane. 

402 



DISEASES OF THE PERIDENTAL MEMBRANE 



403 



ber of arteries and veins (as a rule one main artery and its 
vein, bnt occasionally more than one), passing* through the apical 
foramen into the pulp where it undergoes ramifications ; the other 
two or more arteries and their respective veins are distributed 
to the peridental membrane. They follow in the peridental mem- 
brane a direction parallel to the long axis of the tooth, break- 
ing up into arterioles and capillaries which encircle the mem- 




Fig. 326. — Normal peridental membrane, prepared by carefully detaching the peri- 
dental membrane from a freshly extracted tooth in which no pathologic processes had 
taken place. Notwithstanding the care in dissecting the peridental membrane some layers 
of cementum were removed unsuspectingly and are shown in the section. That scaling 
of root surfaces without removing some of the cementum is an impossibility is confirmed 
by this section, a, a, cementum lamellae; b, b, normal fibers of the peridental membrane. 



brane in its entirety. The peridental membrane is brought into 
close relationship with the gingiva from the crest of the alveolar 
process to the cementoenamel junction, by means of the alveolar 
crest fibers. These fibers run from the peridental membrane into 
the body of the gingiva and are attached to the fibers of the al- 
veolar periosteum as they turn over the crest of the alveolar 
process. In addition, the peridental membrane sends into the 
gingiva the free gingiva groups of fibers, and across the septal 



404 



DENTAL PATHOLOGY 



gingiva the transseptal fibers which run from the peridental 
membrane of one tooth to that of the next. 

The fibers of the peridental membrane are wavy or un- 
dulated in order to enable the tooth to have a certain amount 
of play in its alveolus without traumatization of the fibers. They 
may for convenience of description be divided into the intraal- 




.__£ 



Fig. 327. — Normal peridental membrane in situ, a, dentin; b, b, cementum; c,c, peri- 
dental membrane; d, d, d, cancellated spaces in alveolar process; e, c, e, compact or 
Haversian bone. 



veolar and the extraalveolar fibers. The intraalveolar fibers pass 
into the substance of the cementum and of the alveolus for pur- 
poses of firm attachment, and are the prototypes of Sharpey's 
fibers in periosteum. They comprise the horizontal fibers, the 
oblique fibers, and the apical fibers. 



DISEASES OF THE PERIDENTAL MEMBRANE 



405 



Horizontal Fibers. — Horizontal fibers are a narrow group of 
fibers attached to the cementum at one end and to the alveolar 
process at the other, occupying a space immediately beyond the 
alveolar crest. Their function is to support the tooth against 
lateral displacements, and to assist in preventing rotary move- 
ments of the tooth. 




Fig. 328. — Normal peridental membrane and its relation to cementum and alveolar 
process, a, a, peridental membrane; b, b, cementum; d, d, lamellae of alveolar process 
(compact or Haversian bone). 



Oblique Fibers. — Oblique fibers run obliquely from the ce- 
mentum to the alveolar bone and constitute the bulk of the mem- 
brane. The attachment of the fibers at the cementum is at a 
higher level than in the alveolar process in the case of the upper 
teeth and at a lower level in the case of the lower teeth. Their 
function is to support the tooth against occlusal impactions. Some 
of these fibers run direct to the alveolar process without split- 



406 DENTAL PATHOLOGY 

ting into smaller fibrillar ; others split into fibrillar which are 
joined together for attachment at the alveolar process. 

Apical Fibers. — Apical fibers are a continuation of the oblique 
fibers which, by altering their course for a more direct approach 
to the alveolar process, assume a fan-like distribution. Around 
the apical area of the tooth these fibers, together with the con- 
nective-tissue cells between them and blood vessels and nerves, 
constitute the periapical tissiies. 

The extraalveolar fibers comprise the alveolar crest fibers, the 
free gingiva fibers (unattached at the gingival extremities), and 
the transseptal fibers. 

Alveolar Crest. — Alveolar crest fibers follow for a short distance 
in a direction at right angles to the long axis of the tooth curv- 
ing in an apical direction for attachment at the crest of the 
alveolar process. 

Free Gingiva.— Free gingiva fibers are unattached at their 
terminations in the free gingiva and septal tissues. The group 
which penetrates the septal tissues is known as the septal fibers. 

Transseptal Fibers. — Transseptal fibers take a course immedi- 
ately under the alveolar crest fibers on the approximal aspects of 
the tooth, and are attached to the peridental membrane of the ad- 
jacent tooth. 

This classification of the fibers of the peridental membrane into 
groups is not to be discerned in every specimen studied microscopi- 
cally. It should indeed be accepted pretty much as a theory which 
satisf actorily explains the forces which tend to maintain the tooth in 
its alveolus and enable it to have a limited movement in certain di- 
rections. In the average sectioned specimen of peridental mem- 
brane in situ this arrangement of its fibers can not be discerned 
at all, or only with considerable difficulty. That some such ar- 
rangement as above described actually occurs and is micro- 
scopically visible, there is no doubt; but the variations therefrom 
in arrangement and disposition are also numerous. 

The Structural Constituents of the peridental membrane are: 

1. White fibers, i.e., apical, oblique, horizontal, alveolar crest, 
transseptal and free gingivae, the latter including the septal 
fibers. 

2. Fibroblasts, i.e., spindle-shaped connective-tissue cells occu- 
pying positions parallel to the long axis of the tooth or almost 
any other direction. 



DISEASES OF THE PERIDEXTAL MEMBRANE 407 

3. Cementoblasts — cementum-building cells — located on the ce- 
mentum side of the membrane. 

4. Osteoblasts — alveolar tissue building cells — located on the 
alveolar side of the peridental membrane. 

5. Osteoclasts — alveolar tissue resorbing cells, large multi- 
nucleated cells lying at points along the alveolar side of the 
peridental membrane. 

6. Cementoclasts — cementum resorbing cells presenting the 
same characteristics as the osteoclasts, but located on the cemen- 
tum side of the membrane and concerned in the process of ce- 
mentum resorption. 

7. Epithelial debris — remnants of the enamel organ. 

8. Blood vessels and nerves. An arterial trunk branches out 
into a number of arteries before it penetrates the tooth. One or 
more of these enters the root canal and the others run up on 
each side of the peridental membrane and branch out into a 
veritable network of capillaries which at the crest anastomose 
with the blood vessels of the gingiva and gums. The nerves fol- 
low an analogous course. Blood vessels also enter the peridental 
membrane from the alveolar process and pass out from the peri- 
dental membrane into the alveolar process, thus affording to the 
peridental membrane a collateral circulation from the alveolar 
bone, rendering it possible for the peridental membrane to live 
after the apical circulation and the anastomoses with the blood 
of the gingivae and gums have been destroyed by infective proc- 
esses or by surgical intervention. 

The fibroblasts are the cells which form the white fibers of 
the peridental membrane. These cells are spindle-shaped and 
their number decreases with age. The cells occupy places be- 
tween the fibers. 

The cementoblasts are the cementum-building cells and are to 
be found between the white fibers of the peridental membrane. 
They are irregular in outline. 

The osteoblasts are the bone-building cells, and those which are 
to be found in the peridental membrane represent the remains of 
a group of cells that were concerned in the building up of the 
alveolar structure. 



CHAPTER XXX 

NONSEPTIC PERICEMENTITIS 

By nonseptic pericemental inflammation is to be understood 
that the peridental membrane or pericementum has become the 
seat of vascular changes following abnormal degrees of irrita- 
tion from which bacterial influences are excluded. It may begin 
at the gingival margin and spread to the entire membrane, or 
at the apex and likewise involve the organ throughout its entire 
extent. 

The causes of nonseptic pericemental inflammation may be 
enumerated as follows: 

Root fillings protruding through the apical foramen, broaches, 
etc. ; the introduction of medicaments into the root canal which 
upon evaporation bring about a degree of irritation from which 
the pericemental fibers are unable to quickly recover; the mal- 
leting of gold fillings; the artificial separation of teeth for op- 
erative purposes; the use of clasps, etc.; the construction of 
fillings which interfere with the normal articulation of the tooth 
with its opponent; the impingement upon the gum and peridental 
membrane by crowns, clasps, clamps, and other appliances; rapid 
movement of teeth for orthodontic purposes. 

The use of any irritating drug which under ordinary circum- 
stances will cause marked irritation of soft tissues in other parts 
of the body, should be avoided in root canal medication, or so 
modified in its degree of concentration as to produce the least 
degree of tissue injury compatible with germicidal efficiency. 
For instance, the irritating effect of an otherwise so efficient a 
germicide as formaldehyde, or such of its preparations as trioxy- 
methylene, is pronounced; formaldehyde in any form disorgan- 
izes protein matter readily, and therefore its employment in 
solutions of strong concentration defeats the purpose for which 
formaldehyde is generally employed in root canal therapeutics. 
Verily it destroys microorganic life, but it does this simultane- 
ously with a partial or complete disorganization, not only of the 
periapical tissues, but also of the surrounding alveolar structures. 

408 



NONSEPTIC PERICEMENTITIS 409 

From the standpoint of practical efficiency, it is not alone neces- 
sary that a chemical substance should invariably kill bacteria, 
but it is likewise of importance that it should do this with the 
least possible impairment of the functions of the healthy cells 
with which the antiseptic must come in contact. AVe surmise 
that the tendency to overlook this point is just the echo of the 
practitioner's bacteriologic conception of inflammatory disorders, 
to the exclusion of the factors that render possible bacterial in- 
vasion with its attendant reactions. 

In the seat of an inflammatory process, whether acute or 
chronic, it is of the utmost importance that the cellular elements 
be maintained at their maximum degree of functional activity 
in order that the defensiveness of the area and the opportunities 
for recovery be at their highest. If the functional efficiency of 
the cells of the periapical tissues is lessened by virtue of hav- 
ing been exposed for some time to substances which coagulate 
their protein contents, or which deoxidize or dehydrate their 
protoplasm, or in some other way alter their physical or chemical 
characteristics, the outcome is bound to be detrimental to the 
future efficiency of the tooth. The effect of strong germicidal 
concentrations upon the delicate periapical tissues, made up of 
the fan-like arrangement of the peridental fibers which begin at 
a point where the surfaces of the root begin to converge to- 
ward the apex, plus blood and nerve supply, and interfibrillar 
connective-tissue cells, is manifested in a series of degenerative 
changes eventually ending in their death. Furthermore, the 
partial or complete interference with the chemical mutations 
in protoplasm results in the presence, in the osseous tissue im- 
mediately surrounding the periapical tissues, of areas of partly 
or completely devitalized bony structure which act as a source 
of continuous irritation to the as yet healthy adjacent tissue, 
so that eventually the resistance to bacterial invasion becomes 
subnormal. There is little doubt that areas which have been 
subjected to the action of strong germicides become at some 
future time, bacteria being available, foci of chronic in- 
fection. As all steps in root canal operations are, in only 
a small number of instances, performed with due regard to strict 
asepsis ; and furthermore, as foci of infection may develop in the 
jaws as the result of bacterial invasion via the circulation and 



410 DENTAL PATHOLOGY 

arising from other focal points in the body, it can not be rea- 
sonably argued that even in the presence of partial disorganiza- 
tion of periapical and osseous tissue the bacteria necessary to 
bring about an acute, subacute or chronic inflammatory process 
are not almost always available in sufficient numbers. As a pos- 
sible means of lessening postoperative complications in root canal 
work, the use of milder concentrations of germicidal agents is 
suggested, so graded as to employ in the neighborhood of the peri- 
apical tissues the weakest possible solution compatible with 
germicidal efficiency. 

Any form of irritation or any abnormal degree of pressure at 
the gingival margin or apex of the root, may give rise to non- 
septic pericementitis. It also results frequently upon extirpa- 
tion of the pulp and is due in such an instance to the tearing 
of the pulp from its connection, with the formation of thrombi, 
and to extravasation of blood into the apical peridental mem- 
brane. The nonseptic inflammation which thus develops, trans- 
lated clinically as pain or tenderness, will persist until such time 
as the coagula will have been taken care of by mononuclear 
leucocytes. When anesthetizing the pulp by the cocain pressure 
method the blood content of the pulp is partly driven into the 
vessels of the peridental membrane and this together with the 
formation of thrombi resulting from the extirpation of the pulp 
brings about not infrequently a painful complication in the shape of 
a nonseptic pericementitis. This is assuming, of course, that bac- 
teria have not invaded the periapical tissues, but that they do is, 
however, the case more frequently than the former. In the case 
of teeth devitalized by means of arsenic, if the arsenical applica- 
tion be not correctly gauged, its absorption into the pericemental 
tissues will give rise to a severe nonseptic pericementitis which 
soon thereafter, however, becomes septic in character. Another 
source of apical traumatic nonseptic pericementitis is to be found 
in frequent and unnecessary manipulations with root canal in- 
struments in the neighborhood of the apical foramen, and the 
forcing of root fillings beyond the apical foramen. 

If the cause or causes of a nonseptic inflammation of the peri- 
dental membrane should persist, in time the result will be the 
development of the septic form of pericementitis. In the case 
of the apical form of nonseptic pericementitis a dentigerous cyst 



NONSEPTIC PERICEMENTITIS 411 

may be the ultimate result. It is uot an infrequent occur- 
rence for the area of nonseptic inflammation in the peridental 
membrane to become infected by microorganisms which gain ac- 
cess to it via the circulation. The accidental perforation of a 
root with a drill may give rise to a nonseptic pericementitis even 
though the instrument was a sterile one. This is, however, rarely 
the case, and instead a septic pericementitis results, accompanied 
by the absorption of an area of cementum and of dentin im- 
mediately surrounding the perforation, and of the gum tissue 
which proceeds until the area of absorption is completely ex- 
posed at the gingiva. The passage, accidental or intentional, of 
root canal instruments and filling materials through the apical 
foramen, only rarely results in a nonbacterial inflammation. The 
lowering of the vital resistance of the periapical tissues conse- 
quent upon a continued irritation, chemical or mechanical, soon 
results in their invasion by bacterial forms. 



CHAPTER XXXI 

SEPTIC PERICEMENTAL INFLAMMATION AND ACUTE 
AND CHRONIC DENTOALVEOLAR ABSCESS 

Septic pericemental inflammation may be acute or chronic and 
is caused by the presence in the periapical tissues of microor- 
ganisms which, in the vast majority of instances, have gained 
access to that territory via the root canal. If the bacteria are in 
sufficient numbers and their virulence is relatively high, and if, 
on the other hand, the resistance of the individual and particu- 
larly of the invaded tissue cells is unequal to the task of success- 
fully combating the invasion, an acute dentoalveolar abscess will 
in all probability result. If the reverse should obtain, the dis- 
turbance in the peridental membrane will be slight, and the in- 
fection will be overcome with no permanent injury to the peri- 
dental membrane. In such a case the bacteria will be destroyed 
by the polymorphonuclear leucocytes with horseshoe-shaped or 
partite nuclei. The small destruction of peridental fibers will 
be replaced by cells which proliferate from the preexisting fixed 
fibers of the membrane, while the unaffected leucocytes will enter 
the lymph stream in the perivascular lymph spaces, and the dead 
leucocytes and fixed tissue cells will be carried away in a similar 
manner. In other words, the bacteria having been disposed of 
and their toxins neutralized, a repair of the limited destruction 
of cells takes place and conditions return to normal. 

If the invading bacteria are of low virulence from the begin- 
ning, or folloAving the subsidence of an acute dentoalveolar ab- 
scess, a chronic dentoalveolar abscess will result, provided, of 
course, that the defensive forces of the body are unable to cope 
with the situation. As explained later in this chapter, all in- 
fections of the peridental membrane via the root canal do not 
result in the formation of abscesses, acute or chronic. It is for 
this reason that the title of this chapter specifies pericemental in- 
fection and acute and chronic dentoalveolar abscess. The pres- 
ence of pyogenic bacteria in the apical region, while leading 
in most cases to the formation of a dentoalveolar abscess, never- 

412 



SEPTIC PERICEMENTAL INFLAMMATION 413 

theless, in some few cases, either because of an optimum of de- 
fensive forces, or of timely preventive measures (so-called abor- 
tive measures — measures intended to reestablish a normal cir- 
culation in the area), the infection in the periapical tissues does 
not advance to the stage of visible pus formation with involve- 
ment of the adjacent cancellated bone of the jaw. 

A pulp may be the seat of suppuration, of putrefaction, or of 
suppuration followed by putrefaction. It is well to remember, 
therefore, that a "decomposed" or so-called "putrescent pulp" 
is the result of a suppurative process, followed in a large num- 
ber of instances by putrefactive changes ; or it may be the re- 
sult of purely putrefactive changes. Suppuration is, of course, 
the result of the infection of a tissue — in this instance the dental 
pulp, by pyogenic and other organisms, whose toxins are capa- 
ble of causing degenerative changes and liquefaction of tissue 
cells. The remains of the dead cells and the extra vasated serum 
offer excellent pabulum for that kind of bacteria (saprophytic) 
which thrive upon dead or disorganized tissue. Saprophytic bac- 
teria gain access to the tissue previously disorganized and de- 
vitalized by the activity of the pyogenic bacteria; or else it is 
possible that the pyogenic cocci, and others among the original 
bacterial exciters, have in themselves the power of further split- 
ting the dead nitrogenous matter; viz., the dead cells of the pulp 
and the dead wandering cells. The end products of the suppura- 
tive process are in this way further broken down. The simplifi- 
cation of dead nitrogenous matter by the activity of saprophytic 
microorganisms is termed putrefaction. 

Basic cadaveric alkaloids, or ptomaines, are produced by the 
decomposition of this dead nitrogenous matter, through the 
agency of saprophytic organisms. Cadaverin, putrescin, neuridin, 
neurin, and methyl guanidin are some of the most important. 1 

In the study of pericemental infections, we should constantly 
bear in mind that the products of nitrogenous decomposition are 
in themselves capable of inciting an inflammatory process. \Yhen 
particles of a pulp which has been the seat of suppuration and 
subsequent putref action, or of putrefaction alone, are forced 
through the apical foramen accidentally or in the course of de- 
fective root canal technic. an acute infection may develop in the 



^iegler: General Pathology, New York, Wm. Wood & Co. 



414 DENTAL PATHOLOGY 

periapical tissues within twenty-four hours thereafter. It is 
probable that the activity of the process is due not only to the 
forcing of pyogenic organisms through the apical foramen, and 
to a change in the oxygen tension in the root canal and peri- 
apical tissues, which confers increased virulence to the faculta- 
tive anaerobic bacteria in the periapical tissues, but also to the 
presence therein of some of the cadaveric alkaloids above men- 
tioned although this latter is not the most important contin- 
gency. The organic contents of the dentinal tubules, viz., den- 
tinal fibrillar and their ramifications, are, of course also subject to 
putrefactive changes. According to Yaughan and Novy, ca- 
daverin and putrescin are capable of producing strong inflam- 
mation and necrosis. In large doses they are poisonous to mice, 
rabbits, and guinea pigs. Cadaverin has been found to produce 
suppuration in the absence of bacteria ; neuridin is one of the 
most common products of putrefaction, and while it is not poi- 
sonous in itself, it develops a toxic action when in association 
with other products of putrefaction. 2 

Neurin, however, which occurs in the putrefaction of human 
flesh is in itself a highly poisonous alkaloid. 

In by far the larger percentage of cases the apical section of 
the peridental membrane is the one first to be attacked by in- 
fection via the root canal. These involvements of the pulp are 
the immediate consequence of neglected dental caries and in 
the absence of the latter disease it is safe to assume that, ex- 
cepting a negligible percentage of cases, septic apical perice- 
mentitis would, of course, not develop. The importance of pre- 
venting the onset and progress of dental caries is the key to 
the prevention of septic infections of the apical peridental mem- 
brane, and of dentoalveolar abscess, either acute or chronic. 

Prophylaxis of Pulp Involvements 

Dental caries is, to a large extent, a preventable disease, and 
the secret of its prevention lies in the thoroughness and per- 
sist once with which the prevailing methods of prophylaxis are 
carried out. While the constitutional factor in dental caries un- 
doubtedly influences the extensiveness and rapidity of the proc- 
ess, it does so, however, only in a small proportion of cases. 



■'Vaughan and Nov} 



SEPTIC PERICEMENTAL INFLAMMATION 415 

What these constitutional predisposing causes are we are un- 
able to state with any degree of defmiteness. Theories have been 
promulgated here and there in the effort to blaze the way to- 
ward a reasonable solution of the problem, but as yet nothing 
bearing the stamp of scientific conviction has been adduced. The 
influence of the mineral constituents of drinking water, the na- 
ture of the food used, climate, soil, the influence of the internal 
secretions, the elaboration within the body and the secretion 
within the oral cavity of substances capable of being split into 
compounds having solving properties on the enamel of the teeth, 
are some of the factors which, have been discussed as having a 
possible bearing upon the prevalence of dental caries. But after 
all, about the only phases of the problem of caries prevention 
about which accurate data are available are the actual steps 
of its production beginning with the dissolution of the conti- 
nuity of the enamel prisms by lactic acid. In other words, 
while we know the steps in the process of caries, Ave are in ob- 
scurity regarding the underlying factors or conditions which 
bring about caries, rapid or slow progressing, or which determine 
an immunity or nonsnsceptibility to this disease. 

Therefore, in the work of caries prophylaxis all measures are 
generally aimed at the ultimate causes responsible for its onset — 
causes of a purely local character and preventable in most cases. 
The continuous supervision of patients from the time of the erup- 
tion of the deciduous teeth, with the view of maintaining the 
surfaces of the teeth in a condition of strict cleanliness, and to 
insure correct occlusion of their permanent successors; the oc- 
casional treatment of the fissures of the molars with silver nitrate, 
if supplemented by the thorough brushing of the teeth upon ris- 
ing, after each meal, and upon retiring, will greatly reduce the 
prevalence of caries. And ipso facto the involvement of the pulp, 
its death by suppuration or putrefaction or both, and the spread- 
ing of the infectious process to the peridental tissues, will like- 
wise be circumvented. 

Etiology of Septic Apical Pericementitis 

The causes of septic apical pericementitis may be enumerated 
as bacteria and bacterial products which have invaded the peri- 
apical tissues proceeding from the root canal inwardly (Figs. 



416 



DENTAL PATHOLOGY 



329-334). They are a combination of the pyogenic organisms 
which have been instrumental in destroying the pulp, and the 
saprophytic organisms which may follow in their wake; and to 
these must be added the products of nitrogenous decomposition. 
The peridental membrane is infected by continuity from the in- 





Fig. 329. — Chronic dentoalveolar abscess 
of an upper lateral incisor with a large 
area of rarefaction. The infectious proc- 
ess involved an adjacent tooth on each 
side. An incompletely filled root canal 
was evidently the cause of the continued 
infection. 



Fig. 330. — Chronic dentoalveolar ab- 
scess, in a lower right first molar involving 
both roots. The source of the infection 
was the incompletely treated and filled root 
canals. 




Fig. 331. — Chronic dentoalveolar ab- 
scess involving the upper first and second 
left bicuspids. The apical portion of the 
root of the second bicuspid has undergone 
absorption. 




Fig. 332. — Three chronic dentoalveolar 
abscesses in connection with upper right 
first and second bicuspids and first molar. 
The root canals were the source of the in- 
fection. 



fection in the root canal. It may also become the seat of an in- 
flammation following the passage through the apical foramen of 
the saprophytic bacteria with the products of their activity, 
which were concerned in the decomposition of a pulp which has 



SEPTIC PERICEMENTAL INFLAMMATION 



417 



succumbed following the infliction of a traumatism, such as a 
blow or the sudden impact upon a hard substance in the course 
of mastication, or the continued action of thermal irritation in the 
absence of external opening in the crown. Occasionally even in 
the absence of dental caries, saprophytic infection of the pulp 
occurs either via the blood stream (i. e., blood vessels of the 
apical peridental membrane), or through imperfections in the 
enamel. In the latter instance, the process has been compared by 
Inglis 3 to the putrefactive decomposition of eggs in the presence 
of apparently unbroken shells. The putrefactive process spread- 
ing from the pulp into the periapical tissues doubtless plays an 




Fig. 333. — Chronic dentoalveolar ab- 
scess in upper first and second bicuspid. 
The root canals were the source of the in- 
fection. 




Fig. 334. — Chronic dentoalveolar ab- 
scesses in upper first bicuspid and second 
molar. The path of the periapical infec- 
tion in the molar lias joined with an in- 
fection also chronic which originated at 
the gum margin. 



indirect role in the development of an acute suppuration. There 
follows a decrease in the vital resistance of the periapical tis- 
sues, and a subsequent infection by pyogenic organisms which 
reach the area by way of the blood stream; or, the bacteria re- 
sponsible for the putrefactive decomposition consist of varieties 
among which some assume parasitic powers by a change of en- 
vironment from a disorganized to a living medium. At any rate, 
the passage of the bacteria concerned in the decomposition of a 
dead pulp, and of the animal alkaloids to which they give rise, 
is soon followed in the periapical tissues by suppuration and 
dentoalveolar abscess formation. 



3 Inglis-Burchard: Dental Pathology, 



418 



DENTAL PATHOLOGY 



The etiology of periapical infection is not, however, limited to 
preexisting infections in the root canal resulting from suppura- 
tion or putrefaction of the pulp, or of a combination of both proc- 
esses. In a number of cases after extirpation of a noninfected 
pulp the periapical tissues become the seat of an infectious in- 
flammation. The infection in these instances has been carried 
beyond the apical foramen by unsterile instruments or dressing 
cotton, or by failure to properly protect the root canal by means 
of the rubber dam against contamination from the saliva. 



— 






Fig. 335. — Chronic dentoalveolar ab- 
scess involving the roots of the upper left 
second bicuspid and upper left first molar. 
The roots did not penetrate the maxillary 
sinus as might be surmised from the pic- 
ture and the maxillary sinus was not af- 
fected. The infectious process involved 
the osseous tissue of the maxilla anterior 
to the external wall of the maxillary sinus. 




Fig. 336. — Chronic dentoalveolar abscess 
involving the upper right central and lateral 
incisors. The chronic osteomyelitis resulted 
in caries of bone over a relatively large 
area. Fully two-thirds of the lateral incisor 
projected into this cavity. 



Again, the periapical tissues may become the seat of an infec- 
tion by continuity from an infection in an adjoining tooth (Figs. 
335, 33G and 337). It is not at all rare to find that one or two 
adjoining teeth on either side of the primarily infected periapical 
peridental membrane have become involved. The infectious proc- 
ess spreads through the cancellated spaces to an adjoining tooth 
and from there it may involve one or two teeth more. Infec- 
tion of the peridental membrane, with acute dentoalveolar ab- 
scess formation as the consequence, may also occur from an in- 
fection which, beginning at the gum margin, advances toward the 
apical region. Here the infection involves the pulp which, how- 
ever, does not succumb at once in all instances. One of this type 



SEPTIC PERICEMENTAL INFLAMMATION 419 

of cases showed a well-marked area of rarefaction in the apical 
region, and when examined clinically by percussion, gave every 
indication of being the seat of a chronic dentoalveolar abscess. 
The tooth was opened into, but not before having to resort to 
novocaine anesthesia, much to the intense surprise of the operator 
and the discomfort of the patient. The pulp was removed and 
this was followed by a discharge of pus. The pulp had main- 
tained its vitality in spite of the suppurative process in the peri- 
apical region, probably through an attenuated connection with 
its source of blood and nerve supply. 

Septic pericementitis, acute or chronic, is also caused by per- 
forations of the Avails of root canals by drills, burs, etc., (Figs. 
338-339), or by the passage through the apical foramen of in- 
fected broaches or drills (Fig. 340). A chronic infection is usu- 




T'ig. 337. — Chronic dentoalveolar abscess (so-called dental granuloma) in connection 
with an upper left first and second bicuspid. By a process of continuity the infection 
spread to the mesiodmccal root of the adjoining first molar. 

ally the result, located on the lateral aspect of the single-rooted 
teeth and in the bifurcation of bicuspids and the trifurcation of 
molars. In some instances the alveolar process and the gum tis- 
sue from the gingival margin to the perforation disappear (fol- 
lowing the infection of the perforated area of the peridental 
membrane) to the level of the perforation, exposing that much 
of the root surface. Several such cases have come under our ob- 
servation. 

Another interesting cause of alveolar abscess is intraalveolar 
root fractures, caused by external severe traumatisms (Fig. 341). 
We have recently observed two such cases. One of them was in a 
young acrobat, who presented upon the gum between the upper 
left central and lateral incisors a sinus one inch in length parallel 



420 



DENTAL PATHOLOGY 



to the long axis of the face. The alveolar infection was of long 
duration and had been brought about by the intraalveolar frac- 
ture of the root of the lateral incisor, following presumably an 
effort to lift with his teeth some extraordinary weight. The in- 
fection became apparent years after the accident. At times con- 




Fig. 338. — Chronic dentoalveolar abscess in the 
bifurcation of the roots of the lower right first 
molar brought about by the perforation of the 
mesial wall of the posterior root. 



Fig. 339. — Chronic dentoalveolar 
abscess caused by the perforation of 
the distolingual aspect of an upper 
second bicuspid. 



t 



1 



Fig. 340. — Chronic dentoalveolar ab- 
scess caused by a fragment of a broach 
broken in the root canal. 




Fig. 341. — Intraalveolar root fracture 
of an upper right cuspid, which caused a 
chronic infection of long standing. The 
destructive inflammation had produced a 
sinus whose course was through the labial 
alveolar plate. 



ditions would be quiet, at others a discharge would take place 
from the sinus. When examined by the writer the fragment of 
root was found at the mouth of the sinus, and was removed 
with a pair of dressing pliers. The other case was that of a 
woman giving no history of traumatism, but having suffered in- 
tensely from ''an abscess in one of her upper teeth." Two or 



SEPTIC PERICEMENTAL INFLAMMATION 421 

three teeth posterior to the upper left cuspid had been extracted 
to remedy a condition brought about by the intraalveolar frac- 
ture of the upper left cuspid. The extraction of the fractured 
tooth, as expected, resulted in the disappearance of all symptoms 
of infection. 

The foregoing causes may be summarized as follows : 

1. Through the root canal or canals, by a process of continuity, 
following suppuration or putrefaction or both as the result of 
deep-seated dental caries. 

2. Following death of the pulp by traumatisms or thermal irri- 
tation, in the absence of caries or any break in the continuity of 
the hard tissues of the crown but with the development of pu- 
trefactive processes in the dead pulp. 

3. Following the extirpation of a healthy pulp (preliminary ab- 
sence of infection in canal contents), the infection being carried 
to the- periapical peridental membrane in the course of canal in- 
strumentation, or because of insufficient protection against con- 
tamination from the saliva. 

4. By continuity from an infection in an adjoining tooth or 
teeth. 

5. By continuity from an infection of the gingivae the peri- 
apical tissues become infected and a dentoalveolar abscess fol- 
lows. This source of infection may also give rise to pathologic 
reactions in the peridental membrane of the pyorrhea alveola ris 
type. A paroxysmal intensification of the infection which orig- 
inates in the gingival margin results in a form of abscess of the 
investing tissues known as "pyorrhea abscess" or "lateral ab- 
scess." 

6. Through accidental perforation of the floor of the pulp 
chamber or wall of a root canal. 

7. As the result of intraalveolar root fracture. 

Periapical Infection by the Hematogenic Route 

Bacteria may reach the periapical tissues by way of the circu- 
lation and become active in some area of the periapical tissues 
or some other section of the peridental membrane previously 
weakened by mechanical or chemical irritation. This mode of in- 
fection of the peridental membrane, while not of frequent oc- 
currence, is nevertheless not to be overlooked. 



422 DENTAL PATHOLOGY 

There is as much logic in assuming that foci of chronic infec- 
tion upon areas of the body at remote distances from the teeth 
and jaws may bring about infections of the peridental membrane, 
as there is in accepting the possibilities of metastatic infections 
from foci of infection around or upon the roots of teeth. The 
so-called pericemental abscess, first discussed by D. D. Smith, 
and subsequently minutely investigated by Kirk and Darby, is 
a possible instance of infection of the peridental membrane via 
the blood stream. It is of course admitted that the infection in 
these pericemental abscesses in teeth having live pulps may also 
originate at the gum margin, but the clinical evidence in the 
cases described by Kirk points with more definiteness toward the 
hematogenic mode of invasion. The lateral or pyorrheal abscess 
is a pathologic reaction different from the pericemental abscess, 
and is the result of either an exacerbation of an infection in the 
soft tissue of the gum, the bacteria having penetrated through 
the subgingival space, or else of the infection through the epi- 
thelium of the gum tissue overlying the pyorrhea pocket when 
the gingiva has been previously destroyed by the infection. 

Recovery from Periapical Infections. Acute and Chronic 

Processes 

Septic apical pericementitis does not lead in every case, as pre- 
viously stated, to the formation of an acute or chronic dento- 
alveolar abscess. In those instances in which the invading or- 
ganisms are of low virulence and are present in relatively small 
numbers, and when the vital resistance of the invaded tissue cells 
is high, the symptoms of the inflammatory process subside be- 
fore reaching the stage of abscess formation. Again, it should be 
noted that the periapical tissues may be invaded by bacteria 
which from the start give rise to chronic symptoms. For in- 
stance, following the extirpation of a normal pulp, if every step 
of the operation has not been performed with regard to complete 
asepsis there will develop in twenty-four to forty-eight hours 
symptoms of periapical pericementitis. This inflammation is in 
many cases due to the introduction of bacteria into the peri- 
apical tissues in the course of instrumentation. 

These forms of septic apical pericementitis do not always pro- 
gress to abscess formation. One or two conditions account for 



SEPTIC PERICEMENTAL INFLAMMATION 423 

the subsidence of the symptoms. The infection is either entirely 
overcome by the natural defenses of the body, or else all of the 
bacteria are not overcome ; and then, being of low virulence, re- 
main in the periapical tissues and set up a low grade inflamma- 
tion, thus establishing a chronic periapical abscess — a so-called 
blind abscess or, erroneously a dental granuloma, encapsulated 
by a Avail of fibrous tissue. In the former case (viz., when 
the infection is overcome following active phagocytosis) it 
is to be assumed that the bacteria have caused recoverable cell 
degeneration or, at most, the death of so few cells that their re- 
placement by new cells through the agency of fibroblasts is 
readily accomplished. 



CHAPTER XXXII 

ACUTE APICAL DENTOALVEOLAR ABSCESS 

The infection, if it progresses to the point of acute dento- 
alveolar abscess formation in the periapical tissues, because of the 
high virulence of the bacteria and their presence in large num- 
bers, together with the low resistance of the invaded tissue cells, 
advances through the alveolar bone to discharge at some point 
in the mouth, or on the face, or neck, and in rare instances in 
areas of the body even more remote from the original seat of the 
infection. 

An acute apical dentoalveolar abscess may be denned as an area 
of infection localized in the apical region of the peridental mem- 
brane, originating in the vast majority of cases in a preexisting 
infection in a root canal or canals of the corresponding tooth, 
and in a few instances from a previously infected apical area 
of a neighboring peridental membrane. It is at first but poorly 
circumscribed. It develops as readily upon deciduous as upon 
permanent teeth and is in the majority of cases the sequela of 
neglected dental caries. In multirooted teeth the pulp in one, 
and even in two root canals may be alive, while in the remain- 
ing root canal it may have undergone suppuration or putrefac- 
tive decomposition, or both, involving the apical peridental mem- 
brane and resulting in an acute dentoalveolar abscess. 

Such an abscess shows at first evidences of being slightly cir- 
cumscribed. The virulence of the infection — the rapidity with 
which the bacterial toxins destroy the cells with which they come 
into contact, either directly or indirectly — prevents to some ex- 
tent that form of tissue proliferation which eventually results in 
the encapsulation of a focus of infection. Tissue proliferations 
are in inverse ratio to the virulence of the infection, the less 
virulent the infection, the more abundant the tissue prolifera- 
tions; and vice versa. 

From a pathologic standpoint the chronicity or acuteness of an 
in (lamination is not determined exclusively by the relative de- 
gree of virulence of the bacteria, or the severity of the symp- 

424 



ACUTE APICAL DENTOALVEOLAR ABSCESS 425 

toms, or the time consumed by the infectious process up to the 
establishment of a sinus. An inflammation is chronic when the 
amount of connective tissue of repair (fibroblasts) predominates, 
and when among the leucocytes which have been called to the 
seat of the infection the mononuclear variety predominates; it 
is acute when the fibroblasts and the fibers to which they give 
origin are in the minority and the polymorphonuclear leucocytes 
are in the majority. In chronic inflammations the mononuclear 
leucocytes and plasma cells are in the majority, while in the acute 
inflammations the polymorphonuclear leucocytes are in the ma- 
jority. 

Clinical Symptoms 

The symptoms accompanying the development and progress 
of an acute apical alveolar abscess are: 

1. Tenderness of the tooth to percussion and upon mastication. 

2. Pain. 

3. Swelling. 

4. Increased redness of the gum overlying the affected tooth 
and adjacent areas. 

5. Tenderness on pressure on the gums over the apical region 
of the tooth. 

6. Looseness and protrusion of the tooth. 

7. Rise in temperature. 

8. Constipation. 

9. Fetor of breath. 

10. General malaise. 

11. Headache. 

The pain, slight at first, increases gradually in severity; it is 
throbbing in character and is intensified upon assuming a re- 
clining position and does not begin to subside until the im- 
prisoned inflammatory exudates, liquid and solid, reach the soft 
tissues overlying or underlying the affected tooth. Tenderness 
to pressure is in all instances indicative of inflammation of the 
peridental membrane and the greater the area of peridental mem- 
brane involved the more pronounced the tenderness. In severe 
inflammations of the pulp, it might be remarked in passing, either 
septic or nonseptic, the periapical tissues become likewise in- 
volved in the inflammatory process and thus, even in the pres- 



426 DENTAL PATHOLOGY 

ence of a vital pulp, a painful response to percussion may occur. 
This tenderness is in response to stress of occlusion or to per- 
cussion of the tooth for diagnostic purposes. Pain is also due 
to an exaggerated intraosseous pressure, the inflammatory ex- 
udates, liquid and solid, being enclosed in the cancellated spaces, 
freely supplied with blood vessels and nerves. Practically all 
acute dentoalveolar abscesses, if proper measures are not in- 
stituted to remove all sources of infection in the root-canal, be- 
come in time chronic. 

The protrusion of a tooth is caused by infiltration of the peri- 
dental membrane by inflammatory liquid and solid exudates (leu- 
cocytes), and by the swelling of the cells of the peridental mem- 
brane — the cloudy or hydropic degeneration which accompanies 
inflammation in connective tissue.* In the acute form of dento- 
alveolar abscess there is, as a general rule, comparatively little 
destruction of peridental fibers, and consequently these teeth 
frequently recover following correct instrumental and therapeutic 
technic and the filling of the root canals, previously rendered 
aseptic, to the apex. 

With the increase of intraosseous pressure there is an increase 
of pain, increased blood pressure, and a rise in temperature of 
from one to four degrees F. The tongue is thickly furred, the 
breath offensive, and the patient shows evidences of toxemia. 
From twelve to thirty-six hours, but in some cases longer, after 
the pain becomes ivell marked, the infectious process has pro- 
gressed through the cancellated and cortical bone and estab- 
lished an opening through the latter. The inflammatory exudate 
(serum, lymph, degenerated and dead leucocytes and fixed-tissue 
cells) is now under the periosteum, and after the infection has 
brought about a destruction of a small area of the periosteum 
the adjacent soft tissues become involved, and the face swells. 

The gum tissues overlying the root of the affected tooth appear 
red, flabby, and swollen from the beginning of the infection, 
slightly at first, but increasingly so as the infection progresses. 
The extensive swelling of the tissues of the mouth, face and neck 
is not due entirely to diffusion of pus through the tissues, be- 
cause edema enters largely into the process. The cellulitis is 
accompanied by difficulty in opening the mouth, which persists for 
days after the establishment of the sinus. But the difficulty in 



Adami and McCrae: Text Book of Pathology, Philadelphia, Lea and Febiger. 



ACUTE APICAL DENTOALVEOLAR ABSCESS 427 

opening the mouth is due not only to the distention of the tis- 
sues by swelling, but also to involvement of muscular tissue, par- 
ticularly of the masseter and buccinator muscles, which for the 
time being* supplied with an excess of stimulus are maintained 
in a semicontracted state. 

Sinus Formation 

The course of a sinus from a dentoalveolar abscess is governed 
by the location of the affected tooth, upper or lower, in the arch, 
the density of the tissues overlying the seat of the abscess, the 
virulence of the infection, gravity, and the injudicious applica- 
tion of hot poultices (Fig. 342). Acute dentoalveolar abscesses 
in connection with the upper central and lateral incisors and 
cuspids may discharge upon the labial or palatal aspects of the 
maxilla, but, as a general rule, the sinus will open upon the ex- 
ternal, or labial, aspect. Dentoalveolar abscesses in connection 
with the lateral incisor and palatal root of the first molar have 
occasionally been observed to discharge upon the palatal as- 
pect of the jaw. 1 

Sinuses from dentoalveolar abscesses in upper single-rooted 
teeth and in the buccal roots of multirooted teeth discharge, as 
a rule, upon the labial and buccal aspects, respectively; discharge 
upon the palatal side is the exception. 

Dentoalveolar abscesses in connection with the central and 
lateral incisors, cuspids, or first and second bicuspids, may dis- 
charge into the nasal cavity, the sinus opening in the floor of that 
cavity. An abscess upon a cuspid, bicuspid, first, second or third 
molar, may discharge into the maxillary sinus. The shape, size 
and location of the maxillary sinus vary with practically each 
individual; consequently, the relationship of the upper teeth to 
that cavity varies with equal frequency. The upper cuspid, and 
even the lateral incisor, have been known to produce infection 
of the maxillary sinus. 2 

It is of importance to note that bone changes are not always 
visible in cases in which the maxillary sinus has become involved 
by continuity from an infection on the root of the tooth. It has 
been shown by Hunsberg and Hyjek that it is possible to have an 

1 Turner, J. G. : In Science and Practice of Dental Surgery, by X. G. Bennett. 
2 Seydell, E. M. : International Journal of Orthodontia, ii, Xo. 6, 344. 



428 



DENTAL PATHOLOGY 



extension of an infection through the Avails of the frontal and 
sphenoidal sinus to the neighboring parts without macroscopic 
changes in the bone. 3 







Fig. 342. — Result of poulticing the face in connection with acute dentoalveolar abscesses 

(Oakman). 

It is rare that teeth abutting against the floor of the antrum 
have not a thin lamina of bone between the apices of the roots 



3 ibid. 



ACUTE APICAL DENTOALVEOLAR ABSCESS 429 

and the mucoperiosteum of the sinus. If a tooth suspected of 
being the cause of an involvement of the sinus should be extracted 
and no opening should be found leading into the sinus, it is no 
evidence that such a tooth was not at fault. The infectious proc- 
ess may have established a microscopic opening undiagnosable 
by instrumentation. 

Teeth rarely discharge upon the lingual aspect of the mandible, 
because of the greater thickness of bone between the apical areas 
of the teeth and the lingual aspect of the mandible, than toward 
the labial side. A dentoalveolar abscess in connection with any 
one of the lower teeth may "point" externally, gravity being 
to some extent a factor in deciding upon that course of discharge. 
If the infection has followed a course above the origin of the 
deep cervical fascia, the point of discharge Avill be above the 
lower border of the mandible ; but if, on the other hand, the course 
of the infection has been under the deep cervical fascia, the point 
of discharge may be somewhere upon the neck, one or more inches 
under the border of the mandible. In some exceptional cases the 
infectious process has spread under the deep cervical fascia to 
discharge at some point on the chest, and in one case the opening 
of a sinus from a lower tooth was upon the upper third of the 
thigh. Dentoalveolar abscesses in connection with the lower 
teeth, more frequently than any others, discharge externally un- 
der the mandible, establishing submental fistula} (Fig. 343). 

In the case of the upper or lower teeth, particularly if the roots 
are long, the buccinator may act as a barrier against evacuation 
into the mouth, the infection in that event spreading subperios- 
teally and, after causing a rupture of the periosteum at a higher 
or lower point beyond the attachment of the buccinator (accord- 
ing as to whether it is an upper or a lower tooth, respectively), 
involves the overlying soft tissues, causes an interstitial abscess 
among the fascial layers, and discharges at some point on the face 
or jaws. 4 

The symptoms accompanying the involvement of the soft tis- 
sues of the face or neck, in the case of an acute dentoalveolar 
abscess, which will discharge upon the external aspect, are unmis- 
takable. At some area in the swelling in the face or neck the 



4 Turner, J. G.: In "Practice of Dental Surgery," by N. G. Bennett. 



430 



DENTAL PATHOLOGY 



inflammatory symptoms are exaggerated: there is increased red- 
ness, a marked degree of heat to the touch, exquisite tenderness 
to palpation, and toward the last unmistakable fluctuation. 
Following the rupture of the skin the discharge will continue 
until the cause is removed — or else will heal over temporarily, to 
again discharge when exacerbations of the infection occur (sub- 
acute abscess. In the event that the cause is not removed, or is only 




Fig. 343. — Submental sinus. Opening of a sinus from a subacute dentoalveolar abscess 

in a lower incisor. 



partially so, the condition becomes chronic. It may be timely to 
add that a sinus leading from a focus of infection to the ex- 
terior is nature's way of eliminating the infection so far as it 
may be possible without mechanical or surgical interference, and 
a more logical way than that which attempts to drain it through 
the pinhole opening at the apex of the root. 

In some cases the drainage of a dentoalveolar abscess takes 
place through a channel between the alveolar wall and its perios- 



ACUTE APICAL DEN TO ALVEOLAR ABSCESS 431 

teum, and this occurs as well in the case of abscesses upon the 
upper teeth as upon the lower. Abscesses in connection Avith lower 
molars, apparently disobeying the laws of gravity, will discharge 
at the neck of the tooth, owing to the fact that the density of the 
mandible in the region of its border offers a decided resistance 
to the infectious process. 

That stage of a dentoalveolar abscess immediately preceding the 
perforation of the alveolar bone and its periosteum and the in- 
flammatory infiltration of the soft tissues is the one accompanied 
by the most severe pain. The piercing of the periosteum and the 
invasion of the gum tissues and those of the face is marked by a 
subsidence of the pain and an increase in the size of the swelling. 
The invasion of the overlying soft tissues may give rise to a 
small and limited swelling, or to one involving large areas of the 
face and neck. Those abscesses in which streptococci are pres- 
ent in small numbers and staphylococci in large numbers cause 
limited swelling of the soft tissues, while those in which the 
streptococci are present in large numbers give rise to extensive 
involvement of the soft tissues of the Pace and sometimes of the 
neck. Following this stage, the inflammatory discharge pene- 
trates the soft tissues of the gums and of the mucous membrane 
lining the cheeks and spreads into the soft tissues, causing a cel- 
lulitis, viz., a diffused or phlegmonous involvement of soft tissues. 

Phlegmonous inflammation of the face, or facial cellulitis of 
dental origin is. therefore, the result of the involvement by infec- 
tion of the soft tissues of the face and neck, and of the mucous 
membrane of the mouth and marks the last stage of an acute 
dentoalveolar abscess. In some instances the periosteum is not 
perforated at once, but the pus remains under it to find an exit 
at some point remote from the seat of the infection. These sub- 
periosteal abscesses or parities, are 1 lie ones usually causing acute 
or chronic periostitis and osteomyelitis accompanied by limited 
or extensive necrosis. The products of the inflammatory process, 
by reason of a strong resistance of the outer fibrous layer of the 
periosteum, do not find a ready exit into the overlying soft tis- 
sues. The pus remains confined for some time under the perios- 
teum and the infectious process continues subperiosteally causing 
its detachment from the bone and the death of the latter over, in 



432 DENTAL PATHOLOGY 

some cases, large areas. Eventually it will discharge at some 
point distant from the original focus, and in addition to the 
sinus thus formed, other sinuses will lead from the sequestrum 
or sequestra to various points on the face or within the mouth. 
In the absence of early surgical intervention several sequestra 
will be formed and the case may assume alarming proportions. 



CHAPTER XXXIII 

PATHOLOGIC ANATOMY OF ACUTE DENTOALVEOLAR. 

ABSCESS 

A typical dentoalveolar abscess presupposes the death of the 
pulp. The infection of the peridental membrane is caused by 
pyogenic and other organisms previously engaged in the de- 
struction of the pulp with suppuration as the result, and the in- 
fection of the peridental membrane takes place by a process of 
continuity. Once more we are constrained to emphasize that 
saprophytic organisms and the by- and end-products of their 
activity doubtless play some part in the process as previously 
noted. A septic apical pericementitis, in the sense that the in- 
fection is at first not at all circumscribed, precedes the formation 
of a dentoalveolar abscess. 

One of the first symptoms of pericementitis, whether acute 
septic, or acute nonseptic, is tenderness of the tooth to percussion, 
or to any force, no matter how slight, when applied against the 
tooth. This symptom is due to the congestion of the vessels of 
the peridental membrane, the increased amount of blood having 
reached that area in response to the increased stimulus (the ir- 
ritant) whether bacterial, chemical or mechanical. The conse- 
quence is an undue pressure against the sensitive filaments of the 
membrane. The congestion of the blood vessels is the hyperemia 
of the inflammatory cj^cle. As the infection progresses, the tooth 
protrudes in its socket, consequent upon the presence among the 
fibers of the peridental membrane of liquid and solid inflamma- 
tory exudates, and of fibroblasts of repair; this protrusion is 
also the result of the hydropic degeneration of the fibers of the 
peridental membrane. Following a momentary acceleration of 
the blood stream, in the presence of an irritant, slowing takes 
place simultaneously with the rearrangement of the blood cor- 
puscles — the red cells taking a position in the axial stream, the 
leucocytes accumulating in the parietal stream. It is the passage 
into the meshes of the peridental membrane of a serous exudate 
and multitudes of leucocytes, which marks the beginning of the 

433 



434 DENTAL PATHOLOGY 

subconscious struggle on the part of the individual to successfully 
combat the bacterial invasion. 

If the bacteria are in numbers or virulence unequal to the 
power of the body defenses, the symptoms will quickly subside, 
and there having occurred but slight structural derangement, 
conditions will return to normal. Investigations by the author 
have shown him conclusively that such is the termination in some 
cases of mild infection of the peridental membrane. True, a 
comparatively small number of cells may have died, and some 
may have become the seat of degenerative changes. Those in 
which the degenerative changes are slight may recover; those 
in which they are not, succumb, and these few, as well as those 
that had at first died, are carried away, probably in the lymph 
of the perivascular lymph spaces and lymph clefts, and by the 
lymphatics of the cancellated spaces. In the event of an acute 
dentoalveolar abscess developing, all the phenomena typical of 
an acute inflammation in any other region of the body will fol- 
Ioav in sequence with such modifications as the topography of 
the part induces. 

The destructive infectious process affects first the tissues of the 
peridental membrane, then those of the surrounding bony struc- 
ture, then those of the overlying mucous membrane, and finally 
the products of the septic inflammation find an outlet into the 
mouth; or externally onto the face, as under the mandible (sub- 
mental fistula I ; or into the maxillary sinus, in the cases of bi- 
cuspids and molars, and of cuspids, and even of lateral incisors. 
Dentoalveolar abscesses in relation with the central and lateral in- 
cisors and cuspids may discharge into the nasal cavity, and in ex- 
ceptional cases, especially following the use of hot poultices, the in- 
fection may spread between the deep cervical fascia and underlying 
muscular structures to discharge at some point in the body removed 
from the head. In acute dentoalveolar abscess the progress of 
the infection is clinically observable in all of its stages, and its 
symptomatology is definite and unmistakable. Beginning with 
the tenderness of the tooth, the redness of the overlying gum 
tissues, the throbbing character of the pain increasing in in- 
tensity as long as the inflammatory exudates remain imprisoned 
within the unyielding osseous tissue of the jaw, the decrease of 
the pain concomitantly with the perforation and phlegmonous 



PATHOLOGIC ANATOMY OF ACUTE DENTOAL.VEOLAR ABSCESS 435 

involvement of the soft tissues of the month and face — every 
stage can be easily identified. As the tissues of the periapical 
peridental membrane are destroyed following degeneration, 
death, and liquefaction by the action of the proteolytic bacterial 
enzymes, a pathway is established into the osseous tissues of the 
jaw. Here an acute osteomyelitis develops with absorption of 
the cancellated bone, the process continuing through the bone 
until it reaches the periosteum. In the periosteum an acute peri- 
ostitis develops over generally a small area, but should there be 
unusual resistance offered by the toughness and vascularity of 
the periosteum, the infection may here assume a subacute or 
chronic character, several days elapsing before a pathway is 
established into the soft tissues of the face. These subperiosteal 
abscesses, or parules, are rarely of long duration, but in the event 
of their becoming chronic an extensive periostitis and osteomye- 
litis ensues, and with them areas of necrosis in the jaw, upper or 
lower, but more frequently in the latter. The author recalls the 
case of a woman, aged about 45, otherwise in good health, 
except that extensive necrosis developed in the mandible fol- 
lowing an acute exacerbation of a long-standing infection in one 
of the roots of a lower first molar. Several sequestra were re- 
moved at different times during a period of six months or over. 
This patient was in danger of losing the greater portion of the 
mandible, and only timely and judicious surgical and medicinal 
treatment prevented thai serious ending of a pathologic condi- 
tion which at firsl seemed trivial. 

The teeth adjacent to the one which is the seat of an acute 
dentoalveolar abscess may show evidences of being involved in 
the inflammatory process. One or two teeth on each side may 
become tender to percussion and somewhat mobile in their alveoli 
showing that their respective peridental membranes and other 
investing tissues are the seat of inflammatory disturbances. From 
this, recovery is the rule rather than the exception, upon sub- 
sidence of the acute infection in the tooth primarily responsible 
for the infection, following suitable therapeutic or surgical inter- 
ventions. 

The inflammatory serous exudate, together with leucocytes — 
some dead, some in a degenerated condition — and degenerated 
and liquefied fixed tissue cells, are the components of the dis- 
charge known as pus. 



CHAPTEE XXXIV 

CHRONIC DENTOALVEOLAR ABSCESS 
Etiology and Pathologic Anatomy 

By chronic dentoalveolar abscess is understood a continued in- 
fection of low virulence located in any portion of the peridental 
membrane. It may be the result of the persistence, in less degree, 
of an infection which had caused an acute dentoalveolar abscess, 
and again it may exist unpreceded by any acute form of infec- 
tion. A chronic dentoalveolar abscess is in most cases the result 
of the partial removal of the causes responsible for the produc- 
tion of the acute form, through incomplete or defective technic 
or inaccessibility of root canals, or of an extensive destruction of 
periapical fibers by an acute abscess. Following an acute dento- 
alveolar abscess, if treatment is not at once instituted with the 
view to removing the infected contents of the root canal, the 
acuteness of the infection will in time subside, and be followed, 
instead, by a slow type of infection in the periapical tissues and 
adjacent bone areas. The identical result will follow the presence 
of infected pulp debris, through incomplete or defective technic 
or inaccessibilit}^ of root canals, or from an extensive destruc- 
tion of periapical fibers by an acute abscess. A chronic den- 
toalveolar abscess may have a sinus discharging at some point 
in the gum overlying the affected tooth — at the gingival line, 
in the maxillary sinus, the floor of the nose, or at some distant 
point in the mouth or face, or in areas at a distance from the 
focus of infection; or again it may discharge through a root 
canal, or it may have no sinus whatsoever, the latter being the 
so-called "blind abscess" of the older nomenclature to which 
recently the term "dental granuloma" has been given. The 
author inclines to adhere to the old terminology of sinusless 
chronic dentoalveolar abscess, for the reason that pathologically 
it is the reaction to the same character of infection, in a milder 

436 



CHROXIC DEXTOALYEOLAR ABSCESS 



437 



degree than that which produces the acute form of deutoalveolar 
abscess. The stronger infection is characterized mainly by tissue 




Fig. 344.— A chronic clentoalveolar abscess (dental granuloma) attached to the root of 
m upper cuspid. 




Fig. 345. — Chronic deutoalveolar abscess attached to an upper incisor root, a, location 
of apical portion of root; b, b, b, the chronic sinusless dentoalvcolar abscess or so-called 
dental granuloma. 



destruction; the milder, by tissue proliferation (Figs. 344 and 
345). 



438 DENTAL PATHOLOGY 

To the term "granuloma" there exists the objection that for 
many years prior to its adoption by a group of dental writers, 
general pathologists have given it a definite place in the study of 
tissue reactions to specific chronic infections. The term granu- 
loma applies, therefore, to certain tissue reactions brought about 
by bacteria and protozoa whose manifestations are characteris-' 
tically chronic processes, to wit: Bacillus tuberculosis, Bacillus 
leprae, Bacillus mallei, Spirochete pallida, actinomyces, blas- 
tomyces, etc. In these reactions, in the form of masses of mono- 
nuclear wandering cells, surrounded by a wall of fibers and fibro- 
blasts, there is a breaking down when the infection temporarily 
increases in virulence, and metastases follow which exhibit 
the same pathologic characteristics as those of the original in- 
fection. They are modified, of course, by the location and histo- 
logic characteristics of the tissues in which the metastatic mani- 
festation develops, to wit, a tuberculous granuloma, a syphilitic 
granuloma, an actinomycie granuloma, etc., in each instance 
metastatic manifestations characteristic of tuberculosis, syphilis, 
actinomycosis, etc., being apparent. 

It is not so, however, with the tissue reactions to chronic in- 
fections in the apical peridental membrane. These sinusless 
chronic dentoalveolar abscesses — so-called blind abscesses, in the 
sense that they have no external avenue of drainage — Avhen in 
the course of exacerbations of the infection, and following a de- 
crease in the vital resistance of any portion of the body, may 
bring about one of any number of pathologic conditions, e.g., 
arthritis, gastric or intestinal ulcers, nephritis, endocarditis, peri- 
carditis, myocarditis, pernicious anemia, disorders of metabolism, 
neuralgia, neuritis, etc. We shall adhere to the older nomencla- 
ture, and in describing the etiology, pathology, and symptoms, the 
student should bear in mind that the terms "sinusless chronic 
dentoalveolar abscess," or "blind abscess," or "dental granu- 
loma," are used interchangeably. 

To recapitulate, let us say, therefore, that a chronic dento- 
alveolar abscess may assume any one of the following forms: 

1. A chronic dentoalveolar abscess with a sinus. 

2. A chronic dentoalveolar abscess without a sinus — the so- 
called "blind abscess" of the old nomenclature, or dental granu- 
loma. 



CHRONIC DENTOALVEOLAR ABSCESS 430 

3. A chronic dentoalveolar abscess discharging through a root 
canal. 

4. A chronic dentoalveolar abscess with a sinus along the side 
of the root, discharging at the gingival margin. 

In the case of an acute dentoalveolar abscess the short time in 
which the infection remains in the periapical tissues is probably 
the reason extensive detachments of peridental fibers, with conse- 
quent areas of cementum necrosis, occur rarely. The reverse of 
this obtains in the chronic form in which the infection in the 
periapical tissues is kept up from the root canals, causing rela- 
tively extensive detachment and destruction of peridental fibers, 
and areas of cementum necrosis, following exacerbations of the 
infection and the overcoming of the inflammatory elements by 
the reactivated bacteria. These areas of cementum necrosis oc- 
cur in the sinusless chronic dentoalveolar abscess, and also in those 
which discharge through a sinus or root canal. 

There is usually no pain connected with a sinusless chronic 
dentoalveolar abscess, although a sense of heaviness in the affected 
tooth or neighboring teeth may be experienced. Some of the worst 
cases of systemic involvement under tin 4 author's observation from 
sinusless chronic dentoalveolar abscess developed even in eases 
in which the chronic abscesses gave rise to uo symptoms whatso- 
ever, either objective or subjective. 

Early in the course of our studies, before the x-ray was avail- 
able as a routine adjunct in dental practice, our attention was 
centered on a form of a chronic pericemental inflammation in- 
duced by a bacterium apparently of a degree of virulence giving 
rise to chronicity of symptoms. The patients would invariably 
relate a history of pulp necrosis, or of intentional pulp devitaliza- 
tion with subsequent treatment and filling by generally approved 
methods of practice, and very frequently they reported to have 
experienced no degree of discomfort since then. Upon examina- 
tion, both visual and percussive, no definite indication could be 
obtained as to the conditions existing in the periapical tissues ; 
but by locating the upper third of the tooth root and exerting 
pressure with the finger near the apex, a certain degree of tender- 
ness would be elicited in some cases. 

A number of cases, upon being reopened under aseptic pre- 
cautions and upon being subjected to appropriate medication, 



440 DENTAL PATHOLOGY 

would remain in status quo; i. e., conditions would still be as they 
were at the time the suggestion to retreat them was made. 
Neither pain nor any degree of discomfort appreciable by the 
patient had been the warrant for the additional treatment which 
in our opinion seemed to be indicated. These cases were given 
further consideration with the purpose in view of ascertaining, 
if possible, what bearing they could have upon the patient's evi- 
dent decrease in physiologic power — an interruption in the nor- 
mal balance of assimilation, dissimilation and elimination — and 
upon the presence of pain in various regions of the body, of ob- 
scure origin. The subjective symptoms would include such head- 
ings as headaches, lassitude, migraine, indigestion, nephritis, mel- 
ancholia, arthritis, reflex pain, loss in body weight, decreased 
appetite, etc. In some of these cases, hesitating at first to assume 
an ultraradical form of intervention, we endeavored to eliminate 
the infection from the root canals and to refill them completely, 
but even then the results were still unsatisfactory as the systemic 
symptoms continued unabated. In other cases in the same class, 
and as years went on, Ave assumed the positive attitude that in 
the event of failure to restore the teeth to their normal condition 
by the methods of therapeutics at our command, their removal 
would be effected. Needless to add, many cases were there- 
fore sacrificed to the extracting forces, but in so doing the sys- 
temic welfare of the patient was being continuously borne in 
mind, and not the efficiency of his masticatory apparatus. And 
we majr add that in most cases an abeyance of the general sj^mp- 
toms resulted, in many cases so treated complete recovery even- 
tually following. 

Looseness of a tooth which is the seat of a chronic dentoalveolar 
abscess is not invariably present, and in order that it should be 
marked it is, of course, necessary that a decided area of detach- 
ment should have occurred in the apical region of the root. In cases 
of this kind looseness will be perceptible ; otherwise a tooth may 
be the seat of a chronic dentoalveolar abscess and still be firm 
in its socket. 

Percussion as a reliable means of diagnosing inflammations 
of the peridental membrane, either acute or chronic, may be 
advantageously discussed at this time. It is to be regretted 
that the majority of dental practitioners do not avail them- 



CHRONIC DEXTOALVEOLAR ABSCESS 441 

selves of this method of ascertaining the degree of involve- 
ment of the peridental membrane and alveolar bone. The 
tone produced by percussing a tooth with the handle of a metal- 
lic instrument is sharp and acute when the peridental membrane 
is healthy. If the peridental membrane is at all diseased the 
sharpness of the tone is absent, and instead a dull note is pro- 
duced. In percussing a tooth, for instance a central incisor, it 
should be percussed on the lingual surface, on the labial surface 
and on the incisal edge, a molar should be percussed on the 
buccal or lingual surface, and each cusp should be percussed sep- 
arately. If the index finger of the left hand be placed upon the 
gum overlying the root or roots of the tooth percussed, the greater 
the area of rarefaction, if toward the labial or buccal side, the 
greater will be the perception of vibrations by the operator's 
finger. Lately Talbot has discussed percussion as a means of 
diagnosis, and with his conclusions we are in entire harmony, 
having practiced percussion in the diagnosis of pericemental dis- 
ease for many years. 

In the course of pulp suppuration and putrefaction, or both, 
which is the precursor of apical pericemental infection, the tooth 
may become discolored in the majority of cases. The discolora- 
tion varies in intensity, beginning with a slightly pink hue, which 
develops in the stage of pulpitis, and increasing through the reds, 
browns, and blacks of advanced decomposition of hemoglobin, and 
thence to the grays, greens and blacks, the result of chemical 
reactions consequent upon pulp putrefaction. It therefore hap- 
pens that teeth which are the seat of chronic or of acute dento- 
alveolar abscesses exhibit frequently some degree of discolora- 
tion. All pulpless teeth, even when no discoloration has ensued, 
do not possess the same degree of translucency as is the case 
in teeth with live pulps. 

A chronic infection of the peridental membrane, it should be 
here noted, may have for its reaction not only a chronic dento- 
alveolar abscess, but instead in some instances, although rela- 
tively few, cysts may develop; and in these cysts not infrequently 
is to be found evidence of the proliferation of epithelial rem- 
nants of the peridental membrane. Instances of dentigerous or 
root cysts which developed in connection with roots which had 
been the seat of mild chronic inflammations are shown at Figs. 



442 



DENTAL PATHOLOGY 



346, 347, 348, and 349. These, together with their complete his- 
tories, were furnished me by Dr. E. F. Tholen, Los Angeles, and 
some are on record in the periodical literature.* These epithelial 
remnants which were originally observed by Black, and by him 
called at first the glands of the peridental membrane, have since been 




Fig. 346. — Dentigerous or root cyst as- 
sociated in its etiology with a sinusless 
chronic dentoalveolar abscess in an upper 
first bicuspid. 




Fig. 347. — Dentigerous or root cyst 
which extended to the molar region on the 
right side associated in its etiology with 
an injury in the upper right lateral fol- 
lowed by a chronic dentoalveolar abscess. 
The existence of the cyst was ascertained 
nine years after the injury was sustained. 





Fig. 343.— Dentigerous or root cyst as- Fig. 349.— Dentigerous or root cysts 

sociated in its etiology with a chronic associated in etiology with a chronic dento- 

dentoalveolar abscess in an upper second alveolar abscess in an upper first bicuspid, 
bicuspid. 

shown to be the remnants of the enamel organ— the epithelial 
cells of which have become entangled in the peridental tissues 
wherein they remain quiescent until a certain degree of irrita- 
tion leads to their proliferation. Black admitted at no time that 
these epithelial elements were remnants of the enamel organ. 



Pacific Dental Gazette, xxv, p. 7S1. 



CHRONIC DENTOALVEOLAR ABSCESS 443 

stating that he had followed the breaking up of the cells of the 
enamel organ. "I have seen them float away," he says, "with 
the tissues in groups, forming epithelial pearls, some large and 
some very small. I have followed them, from one age of an ani- 
mal to another age, and as I have thus followed them, I have 
found that they were absorbed and disappeared completely." 
The question remains as yet unsolved, although the evidence is 
strongly in favor of the opinion which considers these epithelial 
groupings as derived from the enamel organ. 

Mild chronic inflammation of the peridental membrane brings 
about thickenings of the membrane, circumscribed or diffused. 
These thickenings represent round-cell infiltration, hydropic de- 
generation and proliferation of fixed fibers of the peridental 
membrane. 

Difference in the Pathology of Acute and Chronic Dentoalveolar 

Abscess 

The difference in pathology between acute and chronic dento- 
alveolar abscesses is just the difference in reaction between an in- 
fection leading at once to tissue destruction with little prolifera- 
tion of fibroblasts; and one which, because of low bacterial vir- 
ulence, over a prolonged period of time, brings about an initial 
detachment of the fixed fibers of the peridental membrane on 
the alveolar side with a subsequent Availing off of the infected area 
by fibers which are the proliferations of the fixed fibers of the 
peridental membrane, this structure enclosing large masses of 
mononuclear wandering cells. 

Why the chronic reaction should be termed a granuloma is be- 
yond justification. Neither is it a tumor in the sense of a neo- 
plasm, nor is granulation tissue the characteristic of its contents. 
It is purely the reaction to bacteria of less numbers and of lower 
virulence (actual or relative) than is the case with the acute 
form of dentoalveolar abscess. True that fibroblasts of repair 
may be seen within the circumscribed mass of leucocytes and bac- 
teria ; but they are present in small numbers, and as long as the 
infection persists they play a decidedly insignificant role. The 
essential characteristics are the fibrous envelope and the mono- 
nuclear wandering cells contained therein (Figs. 350-355). These 
cells may be lymphocytes, small and large, mononuclear leuco- 



444 DENTAL PATHOLOGY 

cytes, small and large, and plasma cells in decidedly less numbers 
than any of the other forms. Some polymorphonuclear leucocytes 
are also present. Recently Hartzell, in an exhaustive study of the 
microscopic anatomy of chronic dentoalveolar abscess (dental 
granuloma), 1 asserts that the majority of these mononuclear 
wandering cells are plasma cells. In order to have a clear under- 
standing of the cellular constituents of a sinusless chronic dento- 
alveolar abscess, sections should be studied microscopically under 



Fig. 350. — Chronic dentoalveolar abscess ''so-called dental granuloma"). a, abscess sac; 
b, b, b, round-cell infiltration which constitutes the bulk of the abscess. 

a high power (Fig. 356). A detailed reference to the forms of 
leucocytes that are to be found within the circumscribed mass 
will doubtless aid the student in the task of cell identification in 
a sinusless dentoalveolar abscess (dental granuloma). 

The polymorphonuclear neutrophile leucocytes constitute nor- 
mally about G5 to 70 per cent of the circulating leucocytes in the 
adult, and from 18 to 40 per cent in the child. These cells are 
from 10 to 12 microns in diameter. They are derived from the 
neutrophile myelocytes which are found in bone marrow and 
which are the descendants of the mononuclear myeloblast 



journal of the National Dental Association. 



CHRONIC DEXTOALYEOLAR ABSCESS 



445 



with neutrophile or occasionally eosinopliile granules — a cell sev- 
eral times larger than the polymorphonuclear leucocyte. The 




Fig. 351. — Section of a chronic dentoalveolar abscess (dental granuloma") showing 
a portion of the fibrous wall and of the body of the abscess (granuloma). The fibrous 
wall presents areas of round-cell infiltration similar in their composition to the mass which 
makes up the body of the abscess. The fibrous wall is not an absolute barrier to the in- 
fection, a, fibrous wall; b, round-cell infiltration making up the bulk of the abscess (only 
a small area is shown) ; c, areas of round-cell infiltration in the fibrous wall. 

nucleus in the polymorphonuclear neutrophile leucocyte assumes 
any one of a number of irregular shapes: it may be U-shaped 



446 



DENTAL PATHOLOGY 



with nodular enlargements, or S-shaped and likewise with nodu- 
lar enlargements ; or it may be composed of several separate nu- 




Fig. 352. — Chronic dentoalveolar abscess. High power photomicrograph of a portion of 
the fibrous wall. a> a, fibrous wall. 

clear bodies. The nucleus has an abundance of chromatin fibers. 
These cells are strong phagocytes for bacteria. When found in 
pyogenic discharges these are the so-called pus cells. A some- 



CHRONIC DEXTO ALVEOLAR ABSCESS 



447 



what similar polymorphonuclear form with granular protoplasm 
having a strong affinity for eosin, known as the polymorphonu- 
clear eosinophile, exists in small proportions — from 1 to 2 per cent. 
They are derivatives of the mononuclear eosinophilic myelocyte 
of bone marrow. These polymorphonuclear eosinophiles have 
larger nuclei with coarser fibers than those of the neutrophilic 
forms. They have less phagocytic power than the neutrophile, 
but nevertheless appear early in some acute inflammations. 




Fig. 353. — Chronic dentoalveolar abscess (dental granuloma). Oblique decalcified 
section. The origin of the fibers which form the fibrous wall is from proliferations from 
the preexisting fibers of the peridental membrane, a. a. dentin; b.b, cementum; c, c, 
fibers of the peridental membrane; d, d. beginning of the fibrous wall; c, c, proliferations 
from the preexisting libers of the peridental membrane. 



The lymphocytes which, according to their size, are known as 
small and large, constitute approximately 20 per cent of the total 
number of leucocytes in the normal adult blood, and from 40 to 60 
per cent in the infant. The small are from 5 to 8 microns in diame- 
ter, the large from 8 to 10 microns. Their protoplasm is strongly 
basic, showing as a blue, narrow margin surrounding a clear or 



448 



DENTAL PATHOLOGY 



pale nucleus which takes up most of the cell and which is round, 
or nearly so. The large and small lymphocytes are probably one 
and the same cell, the larger probably being the older. The 
lymphocytes, as well as the mononuclear leucocytes yet to be de- 
scribed, play an unimportant part in chronic inflammations, but 
not so in the acute. They are not phagocytic for bacteria, but 
are so for portions of cells in process of disintegration and foreign 
matter other than bacteria. 



L ^f 




+.< 





Fig. 354. — Chronic dentoalveolar abscess showing marked contrast between hulk of ab- 
scess and fibrous wall, a, a, bulk of abscess; b, b, fibrous wall. 



The large and small mononuclear leucocytes are present in 
from 3 to 5 per cent. The large ones are from 12 to 15 microns, 
therefore larger than even the large lymphocyte. The small ones 
are differentiated from lymphocytes by the nucleus being ec- 
centrically located and not clearly outlined, and surrounded by a 
relatively large amount of protoplasm, as compared with the 
lymphocyte. The protoplasm, which is free from granules, is less 
basophilic than the nucleus. 



CHRONIC DENTOALVEOLAR ABSCESS 



449 



McCallum is of the opinion that all mononuclear wandering 
cells originate from one of three sources : 

d 



f 




1 SSSsS*. 






wm 



___/ 



Fig. 355. — Chronic dentoalveolar abscess (so-called dental granuloma). Longitudinal 
decalcified section. A large number of fibers are seen which have proliferated from the 
fixed cells of the peridental membrane. The fibers at a, a, constitute part of the fibrous 
sac. Groups of fibers are seen at b. b, which penetrate into the chronic dentoalveolar 
abscess for a short distance. The fibers of the peridental membrane at c, c, c, do not 
appear to have been destroyed but merely to have proliferated; d, d, cementum; e, e, 
dentin; f,f,f, areas of round-cell infiltration. The bulk of the abscess would be beyond 
the right of the picture. 



450 



DENTAL PATHOLOGY 



1. The reticulum cells and the endothelial cells of the sinuses in 
lymph nodes, the lymph nodes of the intestine and in the spleen. 

2. From cells which are normally found in the adventitial tis- 




Fig. 356. — High power reproduction of cellular elements in the round-cell infiltration 
in a chronic dentoalveolar abscess (dental granuloma). Mononuclear wandering cells 
predominate, viz., mononuclear leucocytes, lymphocytes and plasma cells; fibroblasts are 
also to be seen. a, a, plasma cells; b, b, b, lymphocytes, c, c, mononuclear leucocytes; 
d, group of mononuclear leucocytes; c, large mononuclear leucocyte; /, polymorpho- 
nuclear neutrophile leucocyte; g, g, fibroblasts. 



CHRONIC DEXTOALVEOLAR ABSCESS 451 

sues of vessels, and scattered elsewhere in the crevices of tissues. 

3. From lymphocytes which emigrate from the blood vessels, 
and in the tissues developed into ameboid forms, quite like those 
already there. 

The origin of the mononuclear forms is attributed by Mallory 
to the endothelial cells of capillaries. The doubt which exists as 
to their source should not mislead the student into considering 
the wandering cells of any kind as of subsidiary diagnostic im- 
portance. Such is by no means the case, as the determination of 
the several classes of leucocytes is essential in the study and 
diagnosis of inflammatory conditions in general, including those 
which develop in the pulp and investing tissues. 

The plasma cell of Unna, a mononuclear wandering cell, is 
probably derived from the lymphocyte. It occurs normally in 
mucous membranes and is present in large numbers in chronic 
and subacute inflammation. Certain peculiarities of the plasma 
cell are constant. The nucleus is surrounded by a halo or vacuole, 
and is located eccentrically. The nucleus has a coarse appearance 
and the protoplasm takes a bluish stain with ordinary nuclear 
dyes. 2 

A chronic dentoalveolar abscess is, as previously stated, the 
reaction to a protracted infection of low virulence, and is consti- 
tuted of a mass of inflammatory cells surrounded by a fibrous 
wall, composed of cells which have proliferated from the preex- 
isting fibers of the peridental membrane. The envelope of the 
abscess is a strong fibrous capsule or sac, within which are to be 
found the inflammatory elements and some fibroblasts; in addi- 
tion, blood vessels are to be found immediately adjacent to and 
within the fibrous cell. The bulk of the dentoalveolar abscess is 
made up of mononuclear leucocytes in large numbers, polymor- 
phonuclear leucocytes in restricted numbers, plasma cells, and a 
few fibroblasts. The capsule does not necessarily mark the bound 
ary of the abscess, for beyond the capsule the author has found a 
continuity of it. 

Trabeculated abscesses are not uncommon, two or more com- 
partments entering into the formation of one single chronic 
dentoalveolar abscess (dental granuloma). 

-McCallum, W. G.: A Textbook of Pathology, Win. Wood & Co. 



452 DENTAL PATHOLOGY 

Bacteria of Septic Pericementitis and Dentoalveolar Abscess 

The organisms concerned in the process of suppurative inflam- 
mation of the periapical tissues are practically the same organ- 
isms as are responsible for the development of suppuration in 
other regions of the body. These organisms are various strains 
of streptococci, the Staphylococcus pyogenes albus, aureus, and 
citreus; and occasionally the cliplococcus of pneumonia. In a 
series of bacteriologic investigations by Schreier, the diplococcus 
of pneumonia was found in large numbers in a series of fifteen 
cases out of a total of twenty. In these infections has also been 
found the organism isolated by Arkovy from gangrenous pulps, 
which he named the Bacillus gangrence pulpce. 

In gangrenous as well as in suppurating pulps, Miller 3 found 
in addition to the foregoing organisms the Bacillus pulpce pyo- 
genes, an organism which occurs either singly or in pairs, or in 
chains of four to eight. It produces liquefaction of gelatin in 
eighteen to twenty four hours from the time of inoculation. The 
same investigator reports finding in a suppurating pulp a thick, 
short bacterium with rounded ends, one and a half to four times 
as long as thick. This organism, designated by him as the Bac- 
terium gingivce pyogenes, liquefies gelatin, and when injected into 
the abdominal cavity of Avhite mice produced death in ten to 
twenty-five hours. 

Recently Gilmer and Moody 4 have obtained from alveolar ab- 
scess and infected root canals, three strains of streptococci. A 
hemolytic streptococcus, producing a wide zone of hemolysis 
was found in the acute form and the Streptococcus viridans and 
a Streptococcus mucosus was found in the chronic forms. These 
three strains, particularly the Streptococcus viridans, grow both 
anaerobically and aerobically. The anaerobic cultures which 
contain streptococci, these investigators found, are rarely pure. 
The streptococcus is rarely found alone, it having been present 
in the infections studied by these investigators in association 
with B. fusif omits. When cultured aerobically only occasionally 
did they find the staphylococcus albus or aureus, the micrococcus 
catarrhalis, and some unidentified saprophytic organism. In two 



3 Miller, W. D. : Microorganisms of the Human Mouth. 

4 A Study of the Bacteriology of Alveolar Abscess and Infected Root Canals, Jour. Am. 
Med. Assn. 



CHRONIC DENTOALVEOLAR ABSCESS 453 

instances they found diphtheroid bacillus which grew both an- 
aerobically and aerobically. 

Additional facts of interest concerning the bacteriology of al- 
veolar abscess and infected root canals are quoted from Gilmer 
and Moody's report: 

"Anaerobically, in old cultures, we have seen in material from 
three different abscesses a black-pigment-producing organism. 
This organism is slow-growing and does not usually appear for 
about five days. We do not believe that it is of any importance 
in these infections. 

"In three of the chronic cases from which material was ex- 
amined the patients were treated with autogenous vaccines with 
striking beneficial results. The vaccines were made from the cul- 
tures of both the aerobic and anaerobic organisms, and were 
given in graded doses at five-day intervals. 

" These were chronic suppurations, following that class of acute 
infections of the mandible characterized by much brawny swell- 
ing, persisting over a week or more with little or no indications 
of pointing. The pus discharge continued with no seeming 
diminution for several weeks after the acute symptoms had sub- 
sided. In each instance the pus flow stopped promptly on the use 
of the vaccine treatment. 

"Those who have made extensive observations of the tendency 
of acute attacks of alveolar abscess recognize that they occur 
epidemically. Whether the epidemics of streptococcus nose and 
throat infections follow or occur simultaneously with epidemics of 
alveolar abscess is a question both of interest and importance. 
We have not sufficient data to warrant a definite statement rela- 
tive to the subject, however, since we have found in both infec- 
tions the same bacteria, and as both occur epidemically, it may be 
discovered that there is a very definite relationship between the 
two infections. 

"It seems reasonable to suppose that the presence of the strep- 
tococcus of nose and throat infections may easily cause simul- 
taneous or secondary infections in the jaws, the organisms reach- 
ing the apices of the roots through cavities of decay in the teeth, 
or through the circulatory channels." 

Rosenow 5 has made cultures from the pus withdrawn from a 



5 Rosenow, E. C. : The Pathogenesis of Focal Infection, Jour. National Dental Assn. 



454 DENTAL PATHOLOGY 



chronic dentoalveolar abscess with sinus and has obtained al 
most pure culture of Streptococci viridans in association with a 
few colonies of Streptococcus hemolyticus. He has also obtained 
from a chronic dentoalveolar abscess a short chained streptococ- 
cus. The cultures from the pulp of the same tooth after extrac- 
tion yielded two days later the same organisms that were isolated 
from the pus of the abscess. 






CHAPTER XXXV 

BONE 

Normal and Pathologic Considerations 

Bone is a form of connective tissue impregnated with lime 
salts. There are two varieties of bone, spongy or cancellated, and 
compact. The spongy bone is the fundamental form, yet only in 
the compact form are all the structural peculiarities of bone 
present. A cross section of compact bone shows a number of 
round openings, the Haversian canals. The central opening of a 
Haversian canal is surrounded by layers of bone concentrically 
arranged — the concentrically disposed lamella— this canal and 
the surrounding lamella' forming a Haversian system. In the 
longitudinal section the course of these canals seems to corre- 
spond to the long axis of the bone, although some run obliquely 
and establish communication between adjacent canals. All the 
Haversian canals communicate with the central marrow cavity 
and may be viewed in the light of continuations from it. Each 
Haversian canal contains bone marrow — myelitic substance — a 
tissue richly supplied with blood vessels, lymphatics and nerves. 
The spaces between the Haversian systems are filled by short 
lamella?, which are not arranged in any definite way — the inter- 
stitial or ground lamella. The circumferential lamellae are those 
which surround the bone on its outer and inner circumference ; 
i.e., they are located immediately under the periosteum and 
around the central marrow cavity. In the ground matrix are 
located the lacuna, from which minute channels radiate — the 
canaliculi. Each lacuna contains connective tissue elements, the 
hone corpuscles. These bone cells exhibit processes which ex- 
tend into the canaliculi. The lacunae of a Haversian system com- 
municate with one another by means of their canaliculi, but not 
with the canaliculi of adjoining systems. The channels through 
the circumferential lamellae which cany blood vessels, lymphatic 
vessels, and nerves from the periosteum to the Haversian canals, 
and those which run across the inner circumferential lamella? to 
the central marrow cavity, are known as Yolkmann's caneds. 

455 



456 



DENTAL PATHOLOGY 



Bone is surrounded by a fibrous membrane, the periosteum. It 
consists of tAvo layers — the outer fibrous, dense protective layer; 
and an inner, less dense layer very rich in blood vessels and com- 
posed of delicate white and elastic fibers. The inner layer is con- 
cerned with the formation of bone and is known as the osteoge- 
netic layer. The outer layer contains the larger blood vessels, the 
inner layer the smaller though more numerous blood vessels. The 
osteoblasts are located in the osteogenetic layer. The fibers of 
Sharpey are fibers from the periosteum which have remained in 
the lamellae without undergoing calcification. The central cavity 
and all cancellated spaces are filled with marrow of which two va- 
rieties are recognized, the red and the yellow, the red being the 
younger variety and the yellow the older. Bone marrow is a 
blood-forming organ and consequently contains all varieties of 
blood cells as well as myelocytes, nucleated red blood cells, giant 
cells, fat cells, mast cells, etc. Bone marrow consists of a delicate 
connective-tissue framework supporting a rich supply of capil- 
laries. The connective tissue cells in marrow are the marrow cells 
which are concerned in bone formation. In yellow marrow, the mar- 
row cells have been replaced by fat cells. In addition there are to 
be found in marrow some large connective-tissue cells — the giant 
cells — which are concerned in the absorption of calcified tissue and 
which are known under the term of osteoclasts. With the ex- 
ception of the bones of the vault of the cranium, of the face, and 
part of the lower jaw, the skeleton is mapped out in its fetal con- 
dition by solid cartilage of the hyaline type. When bone de- 
velops from centers of ossification in cartilage it is known as 
endochondral bone. When formed directly under the perios- 
teum it is known as periosteal bone. The changes evident in en- 
dochondral bone formation consist in an increase in the size of 
the cartilage cells, their rearrangement in rows, and an increase 
in the size of intercellular substance and the deposition of lime 
salts. In endochondral bone formation the process is one of sub- 
stitution: namely, the cartilage cells are absorbed and replaced 
by new bone. In periosteal bone formation the process is car- 
ried out through the agency of the osteogenetic layer. 2 



2 This histological description of bone has been compiled from the writings of G. A. 
Piersol (Textbook of Normal Histology). 



BONE 457 

Bone Involvement in Dentoalveolar Abscess 

If a section of the mandible be examined it will be found that 
it is composed of thick layers of compact bone externally and in- 
ternally and that within the layers of compact bone the cancellated 
or spongy lone is found (Figs. 357, 358, 359, 360, 361, 362 and 363). 
The latter is made up - of the thin bony walls of the cells 
which contain the medullary or nryelitic substance, the so-called 
cancellated spaces. In life these cells are not exactly spaces, be- 
ing almost entirely filled up by the myelitic substances. The char- 
acter of the bone in the walls is identical with that of the compact 
layer which surrounds the mandible in all of its aspects except 
at the upper aspect through which retention is afforded to the 
teeth. The walls of the alveoli, internally, appear more or less 
smooth and are made up of a layer of compact bone, although 
everywhere as seen in ground sections examined microscopically, 
cancellated spaces open through it. Not infrequently some such 
cancellated space will be located on a line with a root canal, and 
consequently when a root canal instrument is forced past the 
apical foramen it will penetrate for a distance without finding 
any obstruction in its way. The alveoli are supported by layers 
of compact bone which are the v alls of the cancellated spaces and 
are so arranged as to afford the greatest possible support against 
direct and lateral stress upon the teeth. 

In the maxilla there is likewise a cortical layer made of com- 
pact bone buccally and lingually, the alveoli of the teeth being 
embedded, so to speak, in the spongy bone between the cortical 
layers. The alveoli here, as in the mandible, are lined internally 
by a semi-compact bone into which open many of the cancellated 
spaces. 

Infections of the periapical tissues invariably lead to varied 
degrees of involvement of the surrounding bony structure. The 
pathologic process which originates within the alveoli, spreads 
to the cancellated substance of the jaw, exhibiting the character- 
istics of an osteomyelitis, but with no tendency, except rarely, to 
spread (Figs. 357, 358 and 359). Osteomyelitis is a destructive 
process affecting the periosteum, the cortex and the marrow? 

The cortical bone lining the alveoli soon breaks down as the 
result of the spreading of an infectious process in the peridental 

3 McCallum: A Textbook of Pathology, New York, Wm. Wood & Co. 



458 



DENTAL PATHOLOGY 



membrane, and upon the establishment of a passage through the 
cortical layer at any particular point, the infection reaches the 
cancellated substance of the alveolar Avails which is, of course, 
continuous with the cancellated substance of the jaw proper. 
The absorption of the cortical bone of the alveoli in the course 
of an infectious inflammation is probably due to the combined ac- 
tion of osteoclasts and of leucocytes, it having been satisfactorily 
shown by a number of investigators that the presence of osteo- 
clasts is not essential to the absorption of bone (Ribbert). 4 




Fig. 357. — Alveolar bone in the periapical region. The section was obtained from the 
alveolar bone around the apex of the root. The lamellae of bone (calcification install- 
ments) are easily observed, also the lacuna' or heme cell spaces. 



The medullary or myelitic substance in the cancellated spaces 
becomes the seat of an inflammation. Through osteoclastic and 
leucocytic action, as previously noted, the hard substance of the 
bone, viz., the walls of the cancellated spaces, disappear; they 
are, so to speak, eaten through, and the Haversian canals are 
made wider. The contents of the spaces, viz., the myelitic sub- 
stance, become the seat of an acute inflammation in which the 
cellular elements typical of this form of inflammation are present. 
In time the inflamed medullary substance, as the result of the 



*Adami and McCrae: Textbook of Pathology, Philadelphia, Lea & Febiger. 



BONE 



459 








Fig. 358. — Transverse section of tooth showing the arrangement of bone in the alveoli. 
The peridental membrane, it will be seen, joins with the medullary substance in the can- 
cellated spaces; a, a, dentin; b, b, cementum; c. c, peridental membrane; d, d, d, d, section 
of compact bone lining alveolus; e, junction of peridental membrane with myeloid sub- 
stance. 



460 



DENTAL PATHOLOGY 




Fig. 359. — Arrangement of cancellated bone in region of central incisors. 




Fig. 360. — Bone of alveolar process and two cancellated spaces. a, a, a, areas of 
compact bone in the cortical layer of an alveolus; b, cancellated spaces; c, c, peri- 
dental membrane. 



BOXE 



461 



action of the liquefying bacterial toxins, breaks down. In some 
places the cortical layer of the alveoli is less than one-third of a 




Fig. 361. — Arrangement of bone in incisal region, showing at a, bone of alveolar septum 
between upper central incisors. 





Fig. 362. — Arrangement of bone in bi- 
cuspid region showing at b, bone of alveo- 
lar septum between the upper bicuspids. 



Fig. 263. — Arrangement of bone in mo- 
lar region, showing at c, bone of alveolar 
septum between upper molars. 



millimeter in thickness. Its involvement and disappearance in 
the direction of thickness is therefore quickly brought about, thus 



462 DENTAL PATHOLOGY 

opening an abundance of pathways for the absorption of bacteria 
and bacterial toxins. 

Acute or chronic apical infections can not therefore be regarded 
from the viewpoint of localized infections. If all acute or chronic 
infections of the periapical tissues do not give rise to systemic 
manifestations, it is not because the products of such infections 
are not in all cases at the portals of absorption, but because the 
individual is able to combat successfully the bacterial invasion. 
It is purely a question of individual resistance or immunity to 
infection. 

Various chains of streptococcus and staphylococcus seem to be 
the predominating bacteria in these lesions, although other or- 
ganisms may bring about the same results in association with the 
staphylococcus and streptococcus, viz., the pneumococcus, ty- 
phoid bacillus, and the fusiform bacillus. The bacteria invading 
the cancellated spaces produce an inflammation of the medullary 
substance, — a myelitis. The cells of the medullary substance 
around the focus of infection are destroyed and their places 
taken by leucocytes which liquefy the necrotic tissues and 
attack the bony lamellae which they reduce to fragments. 5 

Necrosis, Caries and Rarefying Osteitis of the Alveoli and of the 
Jaws. Necrosis of the Apical Areas of Roots 

Necrosis is a term applied to the death of an area of bone tissue 
which is immediately surrounded by living cells. It is death of 
bone en >n<isse. It implies the contemporaneous death of a large 
number of cells and their subsequent separation from the sur- 
rounding healthy bone following an inflammatory process in- 
augurated in the surrounding healthy bone. It is distinguished 
from the process designated as rarefying osteitis, osteoporosis, or 
caries, in that in the case of the latter the individual cells die 
successively. Caries is a term applied to the molecular de- 
struction of bone "corresponding to the ulceration of soft parts." 

In caries both the calcined structure and the organic matrix 
disappear, the former through osteoclastic activity, the latter 
through the action of peptonizing bacterial toxins or by the 
discharge of peptonizing enzymes from the leucocytes, or by both. 



°McC«illuin: A Textbook of Pathology. 

"Stengel and Fox: A Textbook of Pathology, Philadelphia, W. P.. Saunders Co. 



BONE 463 

The causes of necrosis are all those which directly or indirectly 
interfere with the blood circulation in bone. They may be grouped 
as follows : 

1. Mechanical — Blows, accidental traumatism. 

2. Physical — Extreme degrees of temperature. 

3. Chemical — (a) Burns by acids, strong alkalies, ar- 
senic trioxide phenol, formaldehyde, etc. 

(b) The administration beyond the individual's tol- 
erance of mercury, phosphorus, and bismuth. 

4. Bacterial causes — Infections; viz., action of bacteria 
and bacterial toxins and formation of bacterial em- 
boli and infarcts. 

Necrosis follows the obstruction of the blood supply, the re- 
sult of the occlusion of a main artery by an embolus, thrombic or 
infectious. The part dies without its cells undergoing a progres- 
sive degeneration. The infectious emboli play a leading part in 
necrosis of the jaws caused by peridental infections— dentoa-lveo- 
lar abscess, acute and chronic. Masses of bacteria occlude a 
series of capillaries and result in the formation of infarcts in a 
territory adjacent to or slightly removed from the infected tooth 
root. 

Mechanical Causes. — In this group are included causes which in- 
terfere with the blood supply and which result from degrees of vio- 
lence to the jaws. It is well to bear in mind that necrosis in 
the case of bone, and gangrene in the case of soft tissue, results 
from disturbance of circulation whereby the cells do not re- 
ceive the necessary amount of blood or are not properly drained, 
or from disturbances in the cells which prevent them from as- 
similating the required amount of food even though available in 
normal quantity and quality. A blow in the mouth may result 
in such an impact upon the A'essel supplying the peridental mem- 
branes of several teeth as to result in the cutting off of the blood 
supply by emboli, with death of the teeth and eventually their 
exfoliation, and in the death of portions of the surrounding bony 
areas following the formation of occluding thrombi in the injured 
vessels. 

In the group of mechanical causes are also included the necro- 
sis and exfoliation of sections of the alveolar plate following- 
such accidents as falls, bloAvs, fractures during an extraction, etc. 



464 DENTAL PATHOLOGY 

Chemical Causes. — Necrosis of the alveolar bone is occasionally 
the result of destruction of masses of cells by the action of chemi- 
cal agents. The soft tissues of the mouth are likewise liable to 
destruction by this means, particularly following the use of ar- 
senic in the devitalization of teeth. In the event that arsenic 
leaks out from a cavity the soft tissues are first affected, and then 
the underlying bone. Necrosis of the deeper osseous structure 
of the jaws, following the injudicious use of arsenic trioxide, also 
occurs. Unnecessarily large amounts of arsenic in contact with 
the pulp will lead to that result. Too much care can not be ex- 
ercised in the use of this chemical for purposes of devitalizing 
the pulp, particularly so in the case of teeth whose roots are not 
completely developed so that the apical foramina are large. The 
injudicious use of phenol, trichloracetic acid, chromic acid, sul- 
phuric acid, phenolsnlphonic acid or formalin (the last three in 
root canal therapeutics) may cause necrosis in the periapical 
region. 

The careless forcing of acid compounds and strong alkalies 
through the apical foramen is a relatively common source of de- 
struction of periapical alveolar bony tissue immediately surround- 
ing the apex of the root. 

Necrosis of the maxillary bones occurs in those under a mer- 
curial regime and in persons engaged in the manufacture of 
phosphorus matches. Those with carious teeth and diseased gums 
are particularly liable to the form of necrosis caused by phos- 
phorus fumes. It was of frequent occurrence in the early days 
of the manufacture of phosphorus matches. At the present time, 
owing to the care which is given to the teeth and gums of the men 
employed in this industry, the occurrence of phosphorus necrosis 
has been greatly reduced. 

Bacterial Causes. — In this group is included the most frequent 
source of tissue destruction in the roots of teeth and the support- 
ing alveolar structures. An apical abscess, acute or chronic, may 
cause a destruction of peridental fibers which is followed by nec- 
rosis of that portion of the root which is denuded of peridental 
membrane, or in which the peridental membrane has undergone 
retrograde metamorphosis. The process which takes place in the 
root following destruction of the peridental membrane is not 
exactly typical of necrosis, i.e., death en masse, for the reason that 



BONE 



465 



the cementum being devoid of a blood supply of its own is not sub- 
ject to sequestrum formation. Instead it undergoes a molecular 
disintegration equivalent to bone caries, and manifests itself by 
the condition so frequently diagnosed as pathologic root resorp- 
tion (Figs. 364 to 367). The process which occurs in the alveolar 





Fig. 364. — Resorption of the apical areas 
of the root of a lower molar consequent 
upon chronic dentoalveolar abscesses (den- 
tal granulomata) of long standing. 



Fig. 365. — Resorption of the roots of a 
lower right first molar consequent upon a 
chronic infection of the periapical peri- 
dental membrane, the sequela of a septic 

pulpitis. 





Fig. 366. — Beginning of resorption of 
the apical third of a root of an upper cen- 
tral following necrosis of the apical area 
of the root consequent upon a chronic 
dentoalveolar abscess. 



Fig. 367. — A chronic alveolar abscess 
(dental granuloma) in the lower right 
cuspid, right central incisor, left central 
incisor and left cuspid. The apices of 
the roots of the central incisors have un- 
dergone marked resorption. 



osseous tissue in chronic dentoalveolar abscess typifies tissue 
death by consecutive disintegration of cellular elements through 
rarefying osteitis, osteoporosis or caries, practically synony- 
mous terms; or in other words, gradual cell death, as already 



466 



DENTAL PATHOLOGY 



described in the case of osteomyelitis leading to rarefying ostei- 
tis, or to the more complete process of hard-tissue resorption with 
liquefaction of the organic bone matrix — caries of bone (Fig. 
368). Necrosis of areas of alveolar process and jaw bone proper 
is occasionally observed in connection with ulcerative stomatitis. 
The periosteum at the crest, or alveolar border, becomes involved, 




Fig. 368. Chronic dentoalveolar abscess ( dental granuloma) of very long standing in 
which the chronic osteomyelitis which developed in the alveolar process resulted in 
caries of bone in a relatively large area. The apex of the tooth was found to penetrate 
into a cavity in the cancellated substance of the maxilla. 



the infection brings about its detachment, and the involvement 
of the myeloid substance in the cancellated spaces follows. The 
blood supply is cut off from the periosteal side and infectious 
emboli obstruct any number of capillaries in the cancellated 
substance, with necrosis as the result. 



CHAPTER -XXXVI 

PERIOSTITIS OF THE JAW 

Inflammation of the periosteum of the jaw may be acute or 
chronic, depending on the vital resistance of the patient and the 
virulence of the infecting organism. The most frequent causes 
of periostitis of the jaws are : 

1. Acute or chronic dentoalveolar abscess. 

2. Traumatic injuries with or without a communicating ex- 
ternal wound. 

3. Chemical irritation such as may be induced by the continued 
use of mercury or the inhalation of vapors of phosphorus. 

4. As a sequence or in the course of acute or chronic systemic 
infections. 

5. As a sequence to the eruptive fevers and anemia in children. 

6. As the result of tuberculosis or syphilis. 

The acute form of periostitis may be traumatic or infectious, 
although the traumatic form, by establishing areas of decreased 
vital resistance in the periosteum, soon becomes infectious, 
through bacteria gaining access by the hematogenic route in the 
case of traumatism without external communicating injuries, or 
from the outside in the case of traumatisms accompanied by ex- 
tensive breaks in the continuity of the soft tissues. 

In the chronic infectious periostitis in which the bacteria are 
of low virulence, thickening of the periosteum with new bone 
formation in the form of osteophytes and nodular formations, oc- 
curs wherever the osteogenetic layer is stimulated, but, of course 
not where the cells are undergoing degeneration. The infectious 
or suppurative form of acute periostitis may or may not lead to 
necrosis of the underlying bone. If the infected area is speedily 
drained by a sinus, or following surgical interference, necrosis 
will not occur ; but if the reverse should be the case, necrosis will 
result. The infectious inflammation is intraperiosteal or sub- 
periosteal, or both. In the event that no drainage through the 
periosteum is established, the inflammation proceeds between the 
periosteum and the bone, strips the latter of its overlying peri- 

467 



468 



DENTAL PATHOLOGY 



osteum, and necrosis of the superficial layers of bone follows. 
The infection may then penetrate back into the cancellated spaces 
wherein, as the result of multiple infectious emboli (occlusion of 
arterioles and capillaries), interference of the circulation takes 
place, resulting in more extensive areas of necrosis than where 
the periosteum alone is affected. Dentoalveolar abscess is a 
frequent source of periostitis of the jaws accompanied by necro- 
sis and the formation of sequestra (Fig. 369). 

Acute periostitis may be localized or diffused, according to the 
degree of resistance of the tissues immediately over the path of the 




Fig. 369. — Sequestrum which came away attached to a tooth following a chronic dento- 
alveolar abscess of long standing. 



infection, and the type of microorganism concerned in the infec- 
tion. A small area of bone may die ; and again, the process may 
be of a progressive character — a diffuse acute periostitis — caus- 
ing the formation of a number of sequestra over a relatively 
extensive area of the jaw. An acute dentoalveolar abscess re- 
sults usually in a localized acute periostitis, which subsides upon 
the removal of the infectious source in the root canal. The perios- 
titis may, however, be of the diffuse type, accompanied by exten- 
sive necrosis. Acute periostitis, if diffused, results in secondary 
osteomyelitis, causing a greater depth of necrosis of the jaws or 



PERIOSTITIS OF THE JAW 469 

caries of bone. It occurs with greater frequency in the lower than 
in the upper jaw, by reason of the fact that in the upper the blood 
supply is more abundant and anastomosis of blood vessels is 
greater than in the lower. Periostitis is more frequent in chil- 
dren and young persons, inasmuch as it is during childhood and 
early maturity that there is greater susceptibility to dental 
caries (a prolific source of periostitis) by reason of involvement 
of the pulp, and later of the peridental membrane. 

The infection may spread from a root canal into the can- 
cellated substance of the jaws and then into the periosteum 
where it sets up an acute, though limited infection. The symp- 
toms of such a periostitis are as a general rule attributed to the 
infectious process in the peridental membrane and periapical 
structures — the acute dento alveolar abscess. The symptoms are 
masked by the pain incident to the inflammation of the peridental 
membrane and the osteomyelitis in the alveolar bone. If the 
periosteum, at the point through which the infection passes, were 
to be examined, it would be found red and swollen and the area 
around the opening to be the seat of an infiltration by polymor- 
phonuclear leucocytes, some lymphocytes, and by serum and 
lymph. Sometimes the area of periosteum is infiltrated with 
blood. A periapical infection leading to a dentoalveolar abscess 
with involvement of the cortical and cancellated substance of the 
jaw and the soft tissues of the face, induces a periostitis in 
all cases. The opening through the external cortical plate 
of the alveolus into the soft tissues marks the location of the 
area of periostitis. The infection persisting even in a mild de- 
gree, regeneration of the periosteum is prevented and the chan- 
nel leading from the focus of infection to an external opening 
persists until such time as the source of the infection is completely 
removed, and, in abscesses of long standing, until the rarefied area 
as the result of rarefying osteitis and bone caries is curetted and 
mildly stimulated to fill up the loss of osseous tissue. The reten- 
tion of pus subperiosteally is responsible for the death (necrosis) 
and exfoliation of one or more sequestra. Periostitis of the jaws 
may be preceded by osteomyelitis, or vice versa. In the case of a 
spreading pericemental infection resulting in a periostitis, acute 
and of short duration, or in chronic periostitis when the inflamma- 
tory exudates become incarcerated under the periosteum, the peri- 



470 DENTAL PATHOLOGY 

ostitis has been preceded by infectious processes in the substance 
of the bone involving the osseous and medullary substances, viz., 
an osteomyelitis. Again if the pus finds no outlet, owing to the 
resistance of the periosteum, the infection may penetrate back 
again into the bone through the cortical layer, causing a more ex- 
tended osteomyelitis leading to more extensive rarefying osteitis, 
bone caries, or necrosis. 

The commonest form of chronic periostitis is that of syphilitic 
origin. Growth of bone through stimulation of the osteogenetic 
layer occurs. The inflammation must be mild and continuous in 
character in order to result in new bone formation. It can not, 
of course, occur where the cells of the osteogenetic layer have 
undergone degeneration, but, on the other hand, it does take 
place in areas beyond those of degeneration in which the effect 
of the infection does not overbalance stimulation. 

In chronic phosphorus poisoning, periostitis of the noninfec- 
tious type develops at first, but remains as such only a short time. 
The irritation caused by the phosphorus fumes lowers the re- 
sistance of the periosteum and this becomes the seat of bacterial 
proliferation with its sequela?. Fever ; general indisposition ; 
swelling of the gums and face on the affected side ; looseness and 
exfoliation of the teeth ; pus discharges from around the necks 
of the teeth; trismus; sinus or sinuses, intra-oral or extra-oral — 
are some of the most salient symptomatic manifestations of perios- 
titis of the jaws. 

Osteitis is an inflammation of the bone leading to either rare- 
faction or condensation involving the cancellated and compact 
substance of bone. Osteomyelitis affects both the calcined tissue 
and the medullary substance. Osteitis and myelitis invariably go 
together. In the rarefying form the inflammation of the medul- 
lary substance brings about osteoclastic activity, and disappear- 
ance of particles of calcined tissue follows, giving the bone a 
honeycomb appearance. Rarefying osteitis is a chronic process. 
The erosions on an area of bone undergoing rarefying osteitis 
are called Howship's lacunce, in which osteoblasts and giant-cells 
(osteoclasts) are to be seen together. 



CHAPTER XXXVII 
PYORRHEA ALVEOLARIS 

Historical Sketch 

An examination of ancient skulls leads to the belief that the 
earlier races were subject to diseases of the investing tissues of 
the teeth which are very closely allied in pathologic characteris- 
tics to the pyorrhea alveolaris of modern times. The lesions of the 
alveolar process to be seen in many specimens seem to confirm 
the opinion held by most writers on the subject that pyorrhea al- 
veolaris, or some other disease leading to the exfoliation of the 
teeth, dates almost as far back as the human race. Under the 
term "scurvy of the gums" Pierre Fauchard, in 1746, described 
a lesion of the gums beyond the power of therapeutic means to 
eradicate and which invariably terminated in the loss of the 
teeth. 1 

In 1778 Jourdain, in his treatise on diseases of the mouth, de- 
scribes pyorrhea alveolaris under the name of "suppuration con- 
jointe dcs alveoles et eles gencives," namely, a simultaneous sup- 
puration of the alveoli and gums. Toriac, in 1823, seems to have 
been the first writer to suggest the word "pyorrhea," he having 
named the disease "pyorrhee inter-alveolo-dentaire." The term 
was first used by him on the occasion of an oral communication 
to a medical society of Paris. 2 

Oudet, in 1835, recognized the peridental membrane as the seat 
of the disease, and Marechal de Calvi, in 1861, described pyorrhea 
alveolaris with perhaps more clearness than any one of his pred- 
ecessors in the field, and named it ''expulsive gingivitis." Thos. 
Bell 3 , in 1829, recognized two forms of the disease : one of local 
origin with deposits as the exciting cause ; the other of constitu- 
tional origin. Chapin A. Harris, in 1853, in his work, "Principles 
and Practice of Dental Surgery," describes the disease under 
consideration under the heading of "Chronic Inflammation and 



1 Fauchard, Pierre: Chirnrgien dentiste, 1746, i. 

2 Frey, Leon: Pathologic des-Dentes et de la Bouche. 

3 Marshall, J. S.: Operative Dentistry, Philadelphia, J. B. Iyippincott Co. 

471 



472 DENTAL PATHOLOGY 

Tumefaction of the Gums Attended by Recession of Their Mar- 
gins from the Teeth." Harris recognizes a local as well as a 
systemic cause. He says that chronic inflammation of the gums 
may exist for years without being attended by suppuration or 
recession of their margins from the necks of the teeth; but that, 
sooner or later, according to the amount of local irritation and 
the state of the constitutional health and habit of the body, these 
phenomena are developed. With the occurrence of inflamma- 
tion the margins of the gums gradually lose their festooned ap- 
pearance, become thick, spongy and rounded ; and ultimately, on 
being pressed, purulent matter is discharged from between them 
and the necks of the teeth. The sensibility is increased and they 
bleed from the most trifling injury. He describes the possibility 
of constitutional symptoms developing as the result of a local in- 
fection, saying that "more vital organs become implicated and 
the health of the general system is sometimes very seriously im- 
paired." In 1867 Magitot, of Paris, published his views on pyor- 
rhea alveolaris, designating the disease by the term "osteo- 
periostite alveolo-dentaire," and disregarding the role played by 
calcareous deposits in the production of the disease. As the 
antithesis of Magitot 's writings, those of John W. Riggs of 
Hartford, Conn., appeared in 1875. Riggs, after whom pyorrhea 
alveolaris is today designated by some authors as Riggs' disease, 
described the disease as a suppurative inflammation of the gums 
with absorption of the gums and alveolar processes, and he at- 
tributed the disorder to local causes. Dr. F. H. Rehwinkel, in 
1877, called attention to the possibility of pyorrhea alveolaris 
developing in the absence of local factors, and also said that it 
is a hereditary and constitutional disease. Dr. G. V. Black, whose 
investigations of pyorrhea alveolaris appeared in 1866, discussed 
it almost exclusively from the local standpoint — a destructive in- 
flammation of the peridental membrane. Among the most im- 
portant contributors since then to the etiology and pathology of 
pyorrhea alveolaris, the names of Miller, Kirk, Talbot, Darby, 
Truman, Rhein, Hartzell, Hopewell-Smith, Ottolengui, and R. R. 
Andrews, stand out conspicuously. The investigations by Kirk 
on the relation of faulty metabolism to pyorrhea alveolaris and 
pericemental abscess of gouty origin, constitute a series of most 



PYORRHEA ALYEOLARIS 473 

valuable contributions, which the student of the subject should 
consult 4 . 

General Considerations 

The term "pyorrhea alveolaris" is generally accepted as in- 
dicative of inflammatory disorders in the investing tissues of 
the teeth, which if not controlled, eventually end in their ex- 
foliation. The true meaning of the term is "flow of pus from 
the alveolus," and inasmuch as destruction of the peridental 
membrane and alveolar bone, which results in the loss of the 
teeth, is not always attended by a visible flow of pus, the term 
pyorrhea alveolaris is often incorrectly applied so far as true 
pathologic significance is concerned. The loosening and ac- 
tual loss of a tooth is the result of the destruction of prac- 
tically all of the peridental membrane and adjacent alveolar 
bone ; and it thus happens that all pathologic conditions in these 
structures, as well as in the overlying gum tissues, of which the 
prognosis is loss of a tooth by exfoliation, these have come to be 
designated under the generic term, "pyorrhea alveolaris." Many 
terms have been suggested as substitutes for this one, namely, 
phagedenic pericementitis, interstitial pericementitis, Riggs' dis- 
ease, alveolo-dental pericementitis, interstitial gingivitis, gouty 
pericementitis, ptyalogenic calcic pericementitis, dentoalveolitis, 
pyodestructive pericementitis, etc. Not one of these terms, 
however, depicts the series of pathologic phenomena more clearly 
than the commonly employed term, pyorrhea alveolaris, and con- 
sequently no change in the nomenclature seems justifiable at this 
time, at least in favor of any of the previously mentioned names. 

Clinically, several forms of pyorrhea alveolaris are distinguish- 
able. In one form the destructive inflammation in the peridental 
membrane and alveolar process is preceded by varying degrees of ir- 
ritation to the gingivae by salivary calculi; in another, subgin- 
gival calculi are the source of irritation to the structures in- 
volved in the inflammatory process. The etiology of the latter 
form of calcareous deposits has been studied in a preceding 
chapter. Therefore, suffice it to say at this time that subgingival 
deposits do not occur unless the gingiva? have been subjected 



"Arthritism bv E. C. Kirk. Dental Cosmos, July. 1909. 

* Abscesses Upon Teeth with Living Pulps, Dental Cosmos, 1898. 

Pericemental Abscess, Dental Cosmos, 1900. 



474 DENTAL PATHOLOGY 

for some time to irritating stimuli ; that weak, insufficient, or flat 
approximal contacts, the rough edges of crown-bands, of im- 
perfectly inserted fillings, or any other form of mechanical irrita- 
tion; or that chemical irritation which develops consequent upon 
the decomposition of food debris and of the slimy coatings next 
to the gingivae — these are among the most prominent predispos- 
ing causes. In all true forms of pyorrhea alveolaris the bacterial 
factor is to be viewed as the exciter of the inflammatory process 
which causes the loss of peridental membrane and alveolar proc- 
ess, and the exfoliation of the teeth. 

Pyorrhea Alveolaris Caused by Salivary Calculi 

In the form caused by salivary calculi the clinical phenomena 
are not typical of pyorrhea alveolaris, and while it is here dis- 
cussed under that general heading, it should be borne in mind 
that Ave consider that the presence of pockets alongside the roots 
of teeth, which have developed there consequent upon the de-. 
struction of the peridental membrane and alveolar process 
through bacterial activity or through vascular insufficiency lead- 
ing to atrophy, plus bacterial activity, arc the essential phenomena 
of true pyorrhea alveolaris. The pathologic phenomena accompany- 
ing the destruction of the investing tissues by salivary calculi 
are not characterized by the formation of pockets, which if at all 
present are shallow, being not more than two millimeters in 
average depth. The peridental membrane, alveolar process, and 
overlying gum tissue are destroyed to the level of the salivary 
deposit as the result of a combination of pressure atrophy and 
bacterial activity. Consequently, in the salivary calculi form of 
pyorrhea alveolaris (correctly interpreted, the process should 
be termed calcic gingivitis, pericementitis and alveolitis), the 
formation of pockets does not occur, and the degree of suppurative 
inflammation under the deposit, if there should be any, is not pro- 
nounced at any time. Pus forms at a very slow rate, and it is 
seen at the junction of the deposit with the soft tissues, or upon 
the removal of the deposit, Pus is not by any means invariably 
associated with salivary calculi. In those cases in which it is 
present, the suppurative inflammation, in addition to the phe- 
nomena of pressure atrophy, is responsible for the destruction 
of the investing tissues; while in those cases in which no evidence 



PYORRHEA ALYEOLARIS 



475 




Fig. 370. — Subgingival deposits on the root 
surfaces of the lower central and lateral incisors. 
Destruction of the alveolar process and peri- 
dental membrane on the approximal surfaces of 
these teeth, resulting in the formation of so- 
called pyorrhea pockets. 



Fig. 371. — Absence of approxi- 
mal contact accounting for the for- 
mation of a pocket between lateral 
incisor and cuspid. 





Fig. 372. — Absence of contact and pyor- 
rhea pocket formation. 



Fig. 373. — Absence of contact and pyoi 
•hea pocket formation. 




Fig. 374. — Absence of 
pyorrhea pocket formation. 



contacts and 



Fig. 375. — Absence of contact and pyor- 
rhea pocket formation. 



476 



DENTAL PATHOLOGY 



of suppuration is to be detected the investing tissues are de- 
stroyed, probably mainly as the result of vascular interference, 
which leads to atrophy. The appearance of the gum tissues after 
the removal of a salivary calculus is that of an ulcerated surface : 
the tissues are red and swollen, the inflammation immediately 
under the deposit being more severe than in areas not immediately 
in contact with it, They bleed readily, and unquestionably are 
instrumental in the absorption of bacteria and bacterial toxines, 
which are responsible for the onset of systemic disturbances. 











c 












jga 


Pv*' 












^HB;.r7nlJK 


., •' i ■■ 




/L*J&'P/'~;?jBf ■ 


■'QSMKBSnm 



___& 



Fig. 37G. — An area of gingivae, from a pyorrhea pocket, the seat of a chronic inflamma- 
tion. Longitudinal section, a, a, stratified squamous epithelium lining subgingival wall; 
b, h. b, epithelial proliferations, the result of the chronic inflammation involved in the 
tissue; c, c, areas of round-cell infiltration in which the mononuclear wandering cells 
predominate (leucocytes, plasma cells and some mast cells). 



Pyorrhea Alveolaris Caused by Subgingival Deposits 

In the form caused by subgingival deposits (Fig. 370), the de- 
structive inflammation affects the peridental membrane, alveolar 
bone, and gingivae ; but the gum tissue proper, while the seat of 
a chronic inflammation, does not disappear or break down simul- 
taneously with the peridental membrane and alveolar process, 
as is the case in the form caused by salivary calculi. FolloAving 
degrees of irritation to the gingiva} by food impactions which 



PYORRHEA ALVEOLARIS 



477 




Fig. 377. — Gum tissue overlying a pyorrhea pocket decalcified section. Little remains 
to identify the character of the tissue, the major portion of which is now substituted by 
inflammatory wandering cells. Areas of chronic inflammation are seen throughout the tis- 
sue, a, a, a, a, gum tissue; b, b, decalcified area of tooth; c, c, pyorrhea pocket; d.d, 
stratified squamous epithelium from gingival cul-de-sac; e, c. c, large areas of round-cell 
infiltration (predominance of mononuclear wandering cells). 



478 



DENTAL PATHOLOGY 




Fig. 378. — Chronic gingivitis in the gingiva which hy process of continuity will spread 
to the gums and peridental membrane. a, a, cementum; b, b, dentin; c, c, c, stratified 
squamous epithelium lining gingival cul-de-sac; d, large area of round cell infiltration 
(lire-dominance of mononuclear wandering cells). 



! 



PYORRHEA ALYEOLARIS 



479 



find lodgment between the teeth in the presence of either defec- 
tive approximal contacts (Figs. 371, 372, 373, 374, and 375), or 
in the absence of contacts; by neglect of the teeth through in- 
sufficient brushing, etc. ; by the rough edges of fillings or crown 
bands; by salivary calculi; by severe manipulations of ligatures 
and rubber dam clamps ; or by improper handling of the tooth- 
brush, producing injuries of the gingival margins, — an inflamma- 
tory process is inaugurated in these tissues (the free gingivae) ac- 
companied by the depositions of calcareous masses thereunder. 




Fig. 379. — Decalcified transverse section of upper central incisor. In the gum tissue 
a chronic inflammatory process is going on which has resulted in ana-; of tissue liquefac- 
tion. In this instance the chronic gingivitis had not as yet involved the alveolar process, 
although eventually it will do so. a, a, alveolar process; b, b, areas of tissue liquefaction 
in stroma of mucous membrane of gum tissue; c, cementum; d, dentin; e, pulp. 



The subgingival deposits thus produced irritate and subsequently 
bring about an infectious inflammation of the gingiva?, gums, and 
later of the peridental membrane immediately adjacent to them 
(Figs. 376-382). Through the action of liquefying bacterial tox- 
ines the peridental fibers disappear and the infectious inflamma- 
tion, as soon as the crest of the alveolar process is reached, enters 
the bone and there sets up an osteomyelitis with the absorption 
of the bony lamellae (Fig. 383). The inflammation extends again, 



480 



DENTAL PATHOLOGY 




Fig. 380.- — An area of peridental membrane the seat of chronic inflammation in pyor- 
rhea alveolaris. a, decalcified section of tooth; b,b,b, fibers of peridental membrane cut 
at different angles; c, c, c, areas of round-cell infiltration (predominance of mononu- 
clear wandering cells). 



PYORRHEA ALVEOLARIS 



481 




Fig. 381. — Chronic inflammation of peridental membrane. Areas of tissue liquefaction. 
a, a, dentin; b, b, cementum; c, c, c, fibers of peridental membrane; d, d, alveolar process; 
e, c, areas of destruction of peridental fibers (liquefaction). 



482 



DENTAL PATHOLOGY 




Fig. 382. — Transverse section showing o, dentin; b, cementnm; c, peridental mem- 
brane; d, areas of infection in the libers of the peridental membrane which run 
from the cementum of one tooth to the cementum of the adjoining tooth. This picture 
enables us to understand the meaning of infection of the peridental membrane by con- 
tinuity from the gingiva. At c, c. the infection is seen progressing from the direction of 
the gingiva. 



PYORRHEA ALYEOLARIS 



483 




Fig. 3S3. — An infection from the peridental membrane has involved the medullary 
substance in the cancellated space, an osteomyelitis being the result, a, decalcified section 
of tooth; b, b, peridental membrane; c. c. c, alveolar bone; d, chronic inflammation in 
medullary substance of a cancellated space. 



484 



DENTAL PATHOLOGY 



bringing about the deposition of further subgingival deposits 
higher up on the root surface, so that the processes of irritation, in- 
fectious inflammation, and bone resorption consequent upon osteo- 
myelitis, is repeated; and so on until the entire peridental mem- 





Fig. 384. — Destruction of alveolar proc- 
ess and peridental membrane caused by 
food impactions clue to absence of normal 
contact between the upper left cuspid and 
upper left first bicuspid and between the 
latter tooth and the upper left second bi- 
cuspid and between this tooth and the 
upper left first molar. 



Fig. 385. — Destruction of the alveolar 
process and peridental membrane in py- 
orrhea alveolaris, between the upper right 
cuspid and upper right first molar caused 
by a defective bridge restoration. 




Fig. 386. — Absorption of the apical areas of the roots of the upper central incisors 
caused by an infection which had originated at the gingival margin and which had 
caused a large pyorrhea pocket. 



brane and alveolar process are destroyed, and the tooth is exfo- 
liated (Figs. 384-401). In any one of the two forms of pyorrhea 
alveolaris so far described the presence of any systemic disorder 
in the digestive, respiratory or urinary tract, or any chronic 



PYORRHEA ALYEOLARIS 



485 



nervous disorder, or any systemic intoxication of whatever origin 
it might be, acts as the means of "perpetuating" the disease in 




A B 

Fig. 387. — Two radiograms loaned to the author by Dr. T. A. Lynch of Los Angeles. 
These pictures were taken a few hours apart and on account of faulty radiographic 
ttclmic, B shows a marked improvement over the pyorrhea! condition shown in A. The 
"regeneration" of the alveolar process which is shown in the picture on the right side 
is a fictitious result. 





Fig. 388. — Destruction of the alveolar 
process and peridental membrane caused by 
a defective crown impinging upon the 
gingiva. By continuity the infection spread 
to the alveolar septum bringing about its 
partial destruction. In time a deep pyor- 
rhea pocket would result. 



Fig. 389. — Destruction of the alveolar 
process and peridental membrane resulting 
in the formation of a pocket caused by the 
perforation of the distal wall of the root 
of an upper right cuspid. 



the investing tissues. The causes of the pyorrhea alveolaris may 
be of a local character, but the presence of systemic disorders 



486 



DENTAL PATHOLOGY 




Fig. 390. — Destruction of alveolar process and 
peridental membrane in pyorrhea alveolaris con- 
sequent upon chronic osteomyelitis in alveolar 
bone. 



Fig. 391. — Destruction of the al- 
veolar process and peridental mem- 
brane in pyorrhea alveolaris conse- 
quent upon chronic osteomyelitis in 
alveolar bone. 





Fig. 392. — Destruction of alveolar 
process and peridental membrane in py- 
orrhea alveolaris. A deep pocket existed 
between the central incisors and bet 1 
these teeth and the lateral incisors. 



Fig. 393. — Destruction of alveolar proc- 
ess and peridental membrane establishing 
a pocket distal to the first molar. 





Fig. 394. — Extensive pockets involving 
all the roots of lower first and second mo- 
lars. 



Pig. 3')5. — Extensive destruction of al- 
veolar process in pyorrhea alveolaris 
Deep pockets in molar region; subgingival 
deposits are to be seen on mesial surface 
of upper first molar. 



PYORRHEA ALVEOLARIS 



487 



makes it possible for the disease to gain a foothold upon the in- 
vesting tissues such as to render its eradication a problem beyond 
the power of available surgical and therapeutic means. 

Pyorrhea Alveolaris of Systemic Origin 

Any systemic disorder which produces alterations in the quan- 
tity or quality of the blood, such as, for instance, Bright 's disease, 
diabetes, or the uric acid diathesis, tuberculosis, syphilis, etc., 
may act as the systemic predisposing causes of pyorrhea alveo- 




Fig. 39(1. — Pyorrhea alveolaris. Destruction of the alveolar process and peridental 
membrane to a depth of from 5 to 7 millimeters. Distal movement of the affected teeth 
on account of the destruction of the peridental membrane fibers which run from the 
peridental membrane of one tooth to that of the other (transverse fibers). Malocclusion 
had been the predisposing cause of the disease in this case. Observe the absence of the 
greater portion of the gingiva around the affected teeth. Subgingival deposits were present 
upon the mesial, labial, ami distal root surfaces. 



laris. These disorders are reponsible for the lowering of the de- 
fensive forces of the body, and this decrease in vital resistance is 
perhaps nowhere more pronounced than in the investing tissues 
of the teeth ; for, as pointed out by Talbot the peridental mem- 
brane, alveolar bone, gingivae and gums are in the nature of end- 
organs — devoid, or practically so, of collateral circulation, and 
consequently are markedly sensitive to circulatory changes. 

These systemic derangements are to be viewed in the light of 
predisposing causes. They render possible the infection of the 
investing tissues by reason of their having established in those 
structures areas of decreased vital resistance. The bacterial ex- 



488 



DENTAL PATHOLOGY 




Tig. 397. — Pyorrhea alveolaris in the lower teeth in the same case as shown at Fi 
395. Distal movement of the affected teeth. Considerable loss of alveolar bone and pei 
dental membrane between the lower central incisors. 




Fig. 398. — Pyorrhea alveolaris in the upper right cuspid, first bicuspid and first molar. 
Complete destruction of gingiva and destruction of alveolar process and peridental 
membrane for a distance of several millimeters. 



PYORRHEA ALVEOLARIS 



489 



citers are of course present at all times in the mouth, and there- 
fore, following the slightest break in the continuity of the tissues 
consequent upon an injury to the gingival structures, bacteria 
gain entrance ; and the causes which made this possible persist- 




ing. 399. — Pyorrhea alveolaris. Subgingival deposit? were present on the surface of the 
roots in relation with the so-called "pyorrhea pockets." 




Fig. 400. — A typical case of pyorrhea alveolaris. Xote absence of the septal gingivae 
and of the body of the gingiva. The alveolar process for a short distance beyond the 
crest was also absent. 



ing, the peridental membrane and alveolar bone eventually be- 
come involved. The foregoing description applies to a group of 
cases in which treatment by instrumentation is of only temporary 
value unless it is carried out at frequent enough intervals to 



490 



DENTAL PATHOLOGY 



prevent the recurring infection from acquiring an impregnable 
foothold on the tissues. 

The systemic factor is frequently associated, in etiology, with 
a series of local conditions, the same as are responsible for the 
development of the purely local forms of gingivitis and pyorrhea — 
which leads to equivocal conclusions. Under those circum- 
stances frequently the local causes alone are incriminated, when 
as a matter of fact the systemic disorder is frequently just as 
much at fault, The former set of causes incite the disease, the 
latter perpetuate it. 




Fig-. 401. — Destruction of alveolar process in an extensive case of pyorrhea alveolaris. 
Specimen was secured from Anatomical Laboratories of the College of Dentistry, Uni- 
versity of Southern California, and photographed by Dr. A. C. La Touche. 

In another group of cases local causes are apparently absent, 
or if present are not possible of determination unless the operator 
carry out a \exj minute examination of the gingival tissues. The 
infection in these apparently obscure cases frequently originates 
in the subgingival cul-de-sac (subgingival trough), and the initial 
irritation is traceable to the decomposition by putrefaction, fer- 
mentation, or both, of the slimy deposits in proximity to the 
gingival structures. These slimy deposits are particularly evi- 
dent in badly neglected mouths and in those of people who neg- 



PYORRHEA ALVEOLARIS 491 

lect the toilet of their teeth immediately after meals. These de- 
bris consist of a mixture of saliva and food particles. The end 
products of this decomposition, whether alkaline or acid, irritate 
the tissues in the subgingival trough, and infection by the com- 
mon bacterial inhabitants of the mouth soon follows. The in- 
fection, once becoming established, generally persists, notwith- 
standing the most careful and thorough operative and therapeu- 
tic measures. This form of pyorrhea alveolaris originates and 
persists independent of calcareous deposits. Some investigators 
— the late G-. V. Black in particular — incline strongly toward 
the elimination of the systemic factor, attributing to purely local 
causes all the phases and characteristics of the disease. That a 
considerable proportion of cases is of local causation is admitted 
by practically all investigators, but that all cases are of that 
origin has not received, happily, that unanimous acceptance. 

The evidence of clinical observation strongly points to many 
systemic disturbances as etiologic factors in pyorrhea alveolaris. 
Certain forms manifest themselves as complications of digestive, 
renal, or pulmonary disturbances; and again, a form of loosening 
of the teeth is the result of a gradual and progressive atrophy of 
the investing structures of the tooth, occurring in connection 
with arteriosclerosis, atheroma, anemia, etc. In the case of the 
latter group of diseases the loss of the teeth is the result of true 
atrophy of the peridental membrane and alveolar process, due to 
the fact that the gingiva, peridental membrane and alveolar proc- 
ess, being end-organs as previously stated, have their nutrition 
greatly impaired by abnormal changes in the circulatory appara- 
tus. These dental manifestations become evident even before they 
induce manifestations of a more serious nature in any of the vital 
organs. 

Miller, as far back as 1885, submitted a series of investigations 
concerning the bacteriology of pyorrhea alveolaris, and came to 
the conclusion, which holds true today, that pyorrhea alveolaris 
is not caused by any specific bacterium, but is highly polymicro- 
bic in character. Various bacteria are concerned in the process, 
just as is the case with suppurations, in which not only one, but 
various species of bacteria are active. The following is an ex- 
cerpt of Miller's investigations: 



492 DENTAL PATHOLOGY 

''When the disease is so far advanced as to necessitate the ex- 
traction of teeth, we first cleanse the crown and neck of the 
tooth, as well as the adjacent gums, with 5 per cent carbolic acid ; 
and then, after removing the antiseptic with sterilized cotton 
carefully extract the tooth so as not to graze the gums, cheek 
or lips with the apex of the root. A small quantity of pure, 
fresh pus will be found on the root at the border between the 
dead and the living pericementum. I used this matter, as well 
as part of the periosteum of the apex of the root, in my culture 
experiments. In order to obtain in pure culture the bacteria pos- 
sibly contained in the cement-corpuscles or dentinal tubules, I 
placed the tooth for a short time in a sublimate solution of 1 :5000 
(so as to destroy the germs on the surface). Thereupon it was 
rinsed in a large quantity of sterilized water, dried with steri- 
lized blotting-paper, and the outer layers removed with a steri- 
lized knife. Small particles from the deeper layers were then 
scattered on a culture plate. If extraction is not desirable, we 
may proceed in the following manner : The neck of the tooth is 
carefully cleansed and a slight pressure exerted on the gums; by 
this means the desired pus is pressed out between the gums, and 
the neck of the tooth. 

"I made dilution and line-cultures on beef -water peptone 
gelatin of twenty-seven teeth afflicted with pyorrhea alveolaris. 
The gelatin was liquefied in five cases only. Staphylococcus 
pyogenes aureus developed but once; likewise Staphylococcus pyo- 
genes albus. 

"Two formed yellow, one screen coloring-matter; the latter is 
of interest from the fact that it forms no pigment when the access 
of air is prevented; if, however, the liquefied colorless gelatin 
is shaken with air, a beautiful deep green color almost imme- 
diately forms. In most cases I obtained but one kind, or one kind 
so predominated that the rost could be left out of account. In 
Cases 8 and 13 the bacteria cultivated were found to be identical; 
also in Cases 16 and 17. In all the rest they were different; that 
is to say, twenty-seven cases yielded twenty-two different kinds 
of bacteria. 

"From these experiments we might conclude that if there is 
a specific bacterium of pyorrhea alveolaris, it does not readily 
grow on gelatin, a result which is of value in so far as it indicates 



PYORRHEA ALYEOLARIS 493 

that in further experiments on this subject media should be em- 
ployed which admit of being kept at the temperature of the 
mouth. At the same time the thought suggests itself that possi- 
bly the bacterium of pyorrhea alveolaris, like so many mouth bac- 
teria, is cultivated on none of the artificial nutrient media, which 
would of course render all experimenting useless. 

"The few experiments which Avere made on animals resulted 
negatively. The gums of healthy dogs (these animals often suf- 
fer from pyorrhea alveolaris) were slightly detached from the 
neck of the tooth and inoculated with pus, as well as with the 
deposits on teeth attacked by the disease. Slight inflammation 
invariably ensued, in one case also a little suppuration, but in- 
side of a week all cases were completely healed. Further experi- 
ments are necessary to determine whether positive results may 
be gained in the case of old or emaciated and sick dogs. 

"I next made a series of culture experiments on agar-agar, at 
blood temperature. Twelve cases of pyorrhea in human beings 
and six in dogs were examined. I isolated twenty different bac- 
teria from human beings and nine from dogs. Among the twenty 
kinds, Staphylococcus pyogenes aureus was found Twice, Staphy- 
lococcus pyogenes albus once, Streptococcus pyogenes once. Of 
the other sixteen, nine subcutaneously injected produced no particu- 
lar reaction, four a slight, and three a severe suppuration in the 
subcutaneous connective tissue. 

"Among the nine species in dogs, Staphylococcus pyogenes al- 
bus occurred once. Of the other eight, two subcutaneously in- 
jected caused no reaction, five but a slight, and one very profuse 
suppuration, by which large portions of skin were thrown off. 

"I succeeded, consequently, in cultivating a large number of 
bacteria of pyorrhea alveolaris which possessed pyogenic proper- 
ties, but was not able to determine the constant occurrence of any 
particular one which might be defined as the specific microorgan- 
ism of pyorrhea alveolaris. 

"The microscopical examination of stained sections revealed 
masses of different bacteria, cocci and bacilli, and more seldom 
leptothrix, on the surface of the cementum, and where there were 
microscopic cavities in the cementum, or the dentinal tubules were 
exposed in consequence of resorption, the microorganisms were 
found to have penetrated for a short distance." 



494 



DENTAL PATHOLOGY 



M. T. Barrett in collaboration with Dr. Allen J. Smith 5 , in an 
examination of forty-six patients, found endameba bnccalis in 
the contents of pyorrhea pockets, and the absence of endameba in 
seven patients with no recognizable lesion of the peridental mem- 
brane. These findings were taken np by a large number of men 
in the medical and dental professions as satisfactory evidence of 
the pathogenic importance of this parasite in pyorrhea alveolaris. 
That such a conclusion was unwarranted by the findings of Bar- 
rett, Allen J. Smith, Bass, and Johns is now a generally admitted 
fact. Chiavaro 6 , among others has concluded that the endameba 
buccalis, while it is found in the pus of pyorrhea alveolaris, has 
not a pathogenic action ; but to the contrary, as it feeds on bac- 
teria, ''it is most probably an aid to the auto disinfection of the 
mouth. ' ' 

A study of cultures from pyorrhea pockets of forty-seven pa- 
tients by J. Marion Read gives the results shown in the accom- 
panying table : 

WITH 



- ORGANISM 


ALONE 


ONE 
OTHER 


TWO 

OTHERS 


TOTA 


1. Staphylococcus pyogenes albus 


1 


10 


IS 


29 


2. Streptococcus pyogenes 


1 


6 


11 


18 


3. Pneumococcus 




2 


12 


14 


4. Micrococcus catarrhalis 




3 


G 


9 


5. Diplococcus nmcosus 




4 


4 


8 


6. Streptococcus viridans 


3 


3 


1 


7 


7. Staphylococcus aureus 




4 


2 


6 


8. Bacillus nmcosus 




2 


4 


6 


9. Friedlander 's bacillus 




2 


2 


4 


10. Streptococcus nmcosus 




1 


2 


3 


11. Bacillus proteus 






2 


2 


]2. Streptococcus (in short chains) 






2 


2 


13. Bacillus coli 






1 


1 


14. Bacillus prodigiosus 




1 




1 


15. Diphtheroid bacillus 






1 


1 


16. Bacillus pyocyaneus 






1 


1 



5 Barrett and Smith: Dental Cosmos, 1914. 
6 Chiavaro: Dental Review. 



CHAPTER XXXVIII 

PYORRHEA ALYEOLARIS AND PERICEMENTAL 
ABSCESS OF GOUTY ORIGIN* 

With diseases of suboxidation characterized by the presence of 
given amounts of urates of sodium, calcium, magnesium and am- 
monium in the blood, the presence of inflammatory disturbances 
in the investing tissues of the teeth has been associated. 

The "gouty diathesis," or as it is better described by French 
writers, the diathesis of arthritism, is a condition characterized 
by the presence in the blood and tissues of an excess of the prod- 
ucts of the incomplete oxidation of protein bodies in the shape 
of xanthin bases, amido acid compounds, and uric acids. The dep- 
osition of uratic salts upon the roots of teeth seems to occur in 
that diathetic state. Urates are held in solution in the blood by 
virtue of the alkalinity of that fluid, so that when the blood 
passes over an area of decreased alkalinity or of actual acidity, 
the urates are precipitated. These uratic deposits are the source 
of a degree of irritation to the peridental membrane which re- 
sults in the establishment of areas of decreased resistance — a 
locus minoris resist entice — in which bacteria thrive successfully. 
The area of decreased resistance becomes infected by bacteria, and 
suppuration follows. Pus is of a degree of alkalinity greater 
than that of the blood, which fact accounts, according to Kirk, 
for the precipitation of calcium salts upon and around a nucleus 
of uratic deposits. The discharge from this area of infection may 
take place along the gingival margin, this, of course, occurring af- 
ter the infection has destroyed an area of tissue extending from 
the primary seat of the infection to the gum margin. 

The etiology of pericemental abscess — an abscess upon an area 
of the peridental membrane of a tooth containing a live pulp 
and supported by investing tissue whose continuity at the neck of 
the tooth is unbroken — is fundamentally alike to that of pyorrhea 
alveolaris of systemic origin, associated with the uric acid diathe- 
sis. This difference, however, exists : that in pericemental abscess 
the pus discharges into the mouth from an opening in the gum 

*Kirk, K. C. : Abscesses upon Teeth with Living Pulps. Dental Cosmos, 1898. Peri- 
cemental Abscesses, Dental Cosmos, 1900. 

495 



496 DENTAL PATHOLOGY 

tissues opposite the area of infection; whereas, in pyorrhea al- 
veolaris the discharge is at the margin of the gum. Any abscess 
which originates from an infection of the peridental membrane 
secondary to suppuration and putrefaction of the pulp, and which 
discharges into the mouth through a sinus, is not a pericemental 
abscess. By pericemental abscess is definitely understood that 
it is a condition in which an abscess develops upon some aspect 
of the peridental membrane of a tooth having a live pulp. Peri- 
cemental abscesses may be subpericemental or intrapericemental, 
according to whether the destruction of tissue by bacteria has 
taken place under the pericemental membrane, bulging it out, 
and eventually rupturing it, or within the fibrous substance of 
the peridental membrane 1 . 

Etiology and Pathologic Anatomy of Pyorrhea Alveolaris and 
Pericemental Abscess of Gouty Origin 

It is a well known fact that the salts of uric acid are maintained 
in solution in the blood by virtue of the alkalinity of that fluid 
and that they are precipitated by acids, or at least by substances 
of a lower degree of alkalinity than that of the solvent in which 
they are present. Scheele, as early as 1776, had discovered the 
fact that urinary concretions are dissolved by alkalies, and pre- 
cipitated by acids. The application of these known facts to the 
conditions present in the peridental membrane can be made to 
explain the phenomenon of the formation of uratic deposits upon 
the roots of teeth. 

If, as has been previously pointed out, and as does occur, 
uratic salts are precipitated by preference at some point in the 
apical region of the tooth root, it necessarily follows that there 
the fluids and structures must be of a degree of alkalinity less 
than that of the blood. Several years ago, in the course of a de- 
tailed study of pyorrhea alveolaris of gouty origin, this phase of 
etiology was forcefully brought to the author's attention by 
reason of a conspicuous lack of reference in our literature to this 
initial phenomenon in the evolution of that form of pyorrhea. 

Ordinarily, that is to say, under conditions of rest or slight 
activity, all articulations, their ligaments, synovial membranes, 
articulating cartilages, and the fluids in which they are bathed, 



'Kirk, K. C. : Pericemental Abscess, Dental Cosmos, 



PYORRHEA ALVEOLARIS 497 

are of an alkaline reaction; on the other hand, under conditions 
of activity the reaction at once changes to one of less alkalinity 
(relative acidity), or, in extreme cases, to one of actual acidity. 
These reactions of the tissues in question constitute a physiologic 
fact which is frequently demonstrated to students in medical and 
dental schools in the course of their studies of general physi- 
ology, and requires no argument to substantiate its trustworthi- 
ness. A comparatively simple experiment will convince one that 
the reactions are as here stated. After preparing a frog for ex- 
perimentation by first severing the spinal cord at its junction 
with the encephalon, expose the middle articulation of either of 
the hind legs and test the reaction with litmus paper. It Avill be 
found decidedly alkaline. Xow subject the exposed tissues to a 
series of active contractions through electrical stimulation, and 
again test their reaction. It will be found to be markedly acid. 

These changes in reaction, no doubt, also occur in the case of 
the alveolodental articulation. The peridental membrane is com- 
posed of bundles of fibrous connective tissues which, upon being 
subjected to abnormal degrees of irritation, undergo a chemical 
disintegration ending, it is believed, in the production of acid 
compounds. Collagen, the principal element in fibrous tissue, 
when hydrated is converted into gelatin which, upon furl her dis- 
integration, is found to be composed of proteins; these may be 
detected by any one of the known proteic reactions. Proteins, 
upon breaking down during activity, may give rise to sarcolac- 
tic or the plain lactic acid, among other compounds. It is submit- 
ted that the above facts satisfactorily explain the conditions 
which take place in the apical region of the root, and which, in 
the presence of pus-producing organisms, lead to the development 
of a tophus abscess. As an additional argument of the theory 
under consideration, it may be stated that the frequency of gouty 
deposits upon the metatarsophalangeal articulation of the great 
toe is, in the writer's opinion, due to the fact that in the act of walk- 
ing a great proportion of the body's weight is thrown upon that 
part of the foot. The consequence of this strain results in the 
formation of acid substances, and so renders that particular re- 
gion a suitable field for the precipitation of uratic salts. 

It will be seen, therefore, that the initial phenomenon re- 
sponsible for the deposition of uratic salts in any articulation is 



498 DENTAL PATHOLOGY 

the result of a change in the reaction of the tissues brought 
about by the breaking down of protein bodies in the course of 
physical activity, and the consequent formation of acid sub- 
stances. In the case of the alveolodental articulation, whenever 
a tooth is subjected to a degree of activity greater than normal, 
the catabolism of the cellular elements of the peridental mem- 
brane results in the production of acid substances which lessen 
the alkalinity of the membrane, particularly at the point at 
which the greatest degree of stress is felt. In single-rooted teeth 
the uratic deposits are found as a rule in or near the apical re- 
gion of the root, and in multirooted teeth either upon one of the 
roots in a location corresponding to that upon which the uratic 
salts are deposited in incisors, canines, and bicuspids, or else upon 
the bifurcation area. These areas of uratic precipitation are ac- 
counted for by the fact that in the presence of the slightest degree 
of overactivity the locations referred to are the ones which sus- 
tain the greatest degree of stress, for reasons exclusively physical 
and based upon laws of mechanics. Teeth are very often, in fact 
more often than is generally believed, subjected to degrees of stress 
greater than normal. 

A slight deviation from the position which a given tooth should 
occupy in the arch is sufficient to cause that tooth to perform 
an amount of work greater than its normal share should be. 
This leads to overactivity, excessive oxidation, decrease of al- 
kalinity, and probably to the formation of lactic acid through the 
breaking down of the complex protein molecules of the peridental 
membrane, and finally to the precipitation upon the areas under 
greater stress of the uratic salts held in solution in the blood by 
virtue of its alkalinity. 

In a large number of instances of pyorrhea alveolaris, or peri- 
cemental abscess of gouty origin, the main etiologic causative 
factor is the relative or actual acidity of some portion of the peri- 
dental membrane. This is then followed by the precipitation of 
uric acid salts which, acting as an irritant, convert that peridental 
area into a suitable field for the development of pyogenic organ- 
isms. The deposited urates create a locus minoris resistentia?, and 
the pyogenic organisms which find there a suitable field for devel- 
opment are responsible for the formation of pus, which, being 
of an alkalinity greater than that of the blood, causes a precipi- 



PYORRHEA ALYEOLARIS 499 

tation of the calcium phosphates that are frequently found to be 
component of the gouty deposit (Kirk). As the result of the 
infectious process which spreads by continuity to the alveolar 
process and gum tissue, a sinus is established. If the sinus should 
lead directly to and through the guru, a pericemental abscess will 
be established ; if the infection and consequent tissue destruction 
should involve the peridental membrane and alveolar process 
along the side of the root to the neck of the tooth a so-called 
pyorrhea pocket will result. 



CHAPTER XXXIX 

THE DENTAL PULP AND ITS DISEASES 

The dental pulp is the soft tissue contents of the pulp chamber 
and root canals of teeth (Figs. 402 and 403) . It is in close relation 
with the peridental membrane at the apical foramen (Fig. 404). 
It is the remains of the dental papilla — the aggregation of connec- 
tive-tissue cells — supported by a framework of minute fibrillar 
It presides over the formation of dentin during the developmental 
period of the tooth and throughout the life of the tooth in response 
to physiologic and pathologic stimuli. It occupies the pulp 
chamber in the crown of the tooth and the root canal or canals 
in the root of the tooth. Its outline is in a general way that of 
the tooth in which it is contained. It resembles embryonic tissue in 
its delicate fibrillar basis, and in its cells which are round, oval or 
stellate. The dental pulp is proportionately larger the younger 
the individual, and becomes smaller with age as the bulk of dentin 
increases. It is the sensory organ of the tooth and the source of 
the blood and nerve supply of the dentin. After the dentin at- 
tains its full development, the pulp deposits new dentin, through 
the agency of its odontoblasts, under conditions of abnormal 
stimulation and as a physiologic manifestation of increasing age. 

Histologic Constituents 

The histologic constituents of the dental pulp are six, to wit: 

1. Odontoblasts. 

2. Layer of Weil. 

3. Connective-tissue cells. 

4. Intercellular substance. 

5. Blood vessels. 

6. Nerves. 

Odontoblasts. — Odontoblasts are tall, columnar cells lining the 
pulp on the dentin side (Fig. 405). They are about twenty-five 
microns in length and five in width. The nucleus is located to- 
ward the pulpal side, viz., away from the dentin wall. They 
form a protecting layer around the pulp, and from the fact that 

500 



THE DENTAL PULP AND ITS DISEASES 



501 






"..* 




Fig. 402. — A longitudinal section of a normal pulp of man. a, a, a, a, odontoblastic 
layer; b, nerve trunk; c, c, plexus of nerves under odontoblastic layer. The connective 
tissue cells distributed everywhere in the matrix of the pulp are of three kinds, round, 
spindle-shape and stellate. The latter are fewer in number and more difficult to locate. 



502 



DENTAL PATHOLOGY 



they adhere to the walls of the root canals they have been 
collectively named the memhrana eboris. The odontoblastic 
layer of the pulp is the only connective tissue in the body 
having cells of columnar form. This columnar form does not, 
however, persist throughout the life of the pulp. It is particu- 
larly evident prior to and during the formation of dentin; but 
in old pulps, i. e., after dentin has been formed, the odontoblasts 
are round or oval. They are the specific dentin-producing 
cells — a function which they retain throughout the life of the 
pulp. They send processes into the tubules of the dentin — the 




Fig. 403. — Longitudinal section of normal pulp. The same structural elements are to be 
found as are indicated in the previous section. 



dentinal fibrillar or fibers of Tomes, and probably are connected 
among themselves by delicate fibrous processes. 

Layer of Weil. — The layer of Weil is supposed to be that por- 
tion of the pulp lying between the odontoblastic layer on the 
outside, and the portion of the pulp which is thickly studded 
with connective-tissue cells distributed throughout the gelati- 
nous matrix of the pulp on the inside. It itself is described as 
being very sparingly embedded with connective-tissue cells. In 
numerous specimens this layer does not exist, but whether pres- 



THE DENTAL PULP AND ITS DISEASES 



503 



ent or not, is of no physiologic import. Von Elmer lias attributed 
the layer of Weil to shrinkage of the body of the pulp, while 
Wahlkoff considers that the phenomenon is caused by a shrink- 
age of the odontoblasts. It is best studied in transverse sections. 
Connective-tissue Cells. — The connective-tissue cells of the pulp 
are of three shapes — round, spindle-shaped and stellate. In Fig. 



Apical foramen 



- y 



Peridental 
membrane. 



V 



.Bone of alveolar process 



Dentin. 



I Dentin, 



Peridental membrane 



Dentin 



I 



Dentin 



Pulp 

Fig. 404. — Section of a tooth showing relation of the pulp at tbe apical foramen to the 
peridental membrane. Some of the blood-vessels are shown partly tilled with blood cells. 
The fibrillar character of the pulp matrix is seen. 



402 the round and spindle-shaped cells are readily distinguished, 
but the stellate cell is very rare and exceedingly difficult to find, 
being best shown by focusing for depth. 

Intercellular Substance. — The intercellular substance is a gelat- 
inous mass resembling the tissue found in the umbilical cord, 
and known as Wharton's jelly. It is an immature form of con- 



504 DENTAL PATHOLOGY 

nective-tissue consisting of very fine fibrillar Besides these ex- 
tremely slender fibrous elements, connective-tissue fibers of or- 
dinary size are also found supporting the blood vessels and 
nerves. 

Blood Vessels. — The pulp has, relatively speaking, a very rich 
blood supply. During the formative period of the tooth the 
blood is carried to it by means of several arteries. "When the 
development of the tooth is completed the blood supply consists 
as a rule of one small artery and a correspondingly small vein, 
or again the arrangement may consist of three or more arteries 
with their corresponding thin-walled veins entering the tooth 
through one or several foramina. Weil has found that from 
three to ten blood vessels may enter the tooth through the apical 
foramen. The difficulties attending the treatment of roots pos- 
sessed of more than one apical foramen are obvious. This artery, 
or arteries, breaks up into numerous branches which are distrib- 
uted throughout the substance of the pulp, and as these branches 
reach the odontoblastic layer they split into capillary plexuses, 
which lie in close proximity to the odontoblastic cells, from where 
veins carry off the venous blood. The Avails of the vessels of the 
pulp are very thin and easily affected by changes in blood pres- 
sure. 1 

There is no collateral circulation in the pulp, so that any in- 
jury to the blood vessels at the apex affects the vitality of the 
entire pulp. As shown by A. Hopewell-Smith its veins are valve- 
less and noncollapsible. 2 

Noyes has recently demonstrated that lymphatics exist in the 
pulp. 

Nerves of the Pulp. — One or more nerve filaments enter the 
pulp through the apical foramen, each filament being composed 
of from ten to thirty medullated nerve fibers. These nerves 
enter with the blood vessels. After entering the pulp tissues 
they spread out into plexuses and eventually become nonmedul- 
lated, forming rich networks close to the odontoblasts. The 
protoplasmic prolongations of the odontoblasts are the only 
structures which have thus far been demonstrated to enter the 
dentinal tubuli, and until such time as nerve fibrillae can be dem- 



1 IMack, G. V.: Dental Pathology. 

2 Hopewell-Smith, A.: The Histology and Patho-ITistology of the Teeth and Asso- 
ciated Paris, Philadelphia, P. Blakiston's Son & Co. 




Fig. 405. — Section of a pulp of sheep, showing histologic characteristics of odontoblastic 
layer. Section prepared by Dr. A. C. La Touche. 






THE DENTAL PULP AND ITS DISEASES 505 

onstrated within the tubules, the odontoblastic prolongations or 
fibers of Tomes, must continue to be looked upon as the only 
means by which impulses are carried from the dentin to the pulp. 

Fibers of Tomes 

The transmission of sensations from the dentin to the pulp 
takes place through the medium of the fibers contained in the 
dentinal tubuli. These fibers are prolongations of the odonto- 
blasts and while physiologically they play the role of nerves, his- 
tologically they in no way resemble nerve tissue. In addition to 
these processes of the odontoblasts, a process arising from the 
pulp end of the odontoblasts, and a process on each side of the 
cell communicating laterally with the adjoining odontoblasts, 
have been described. These additional processes are not dis- 
cernible in histologic preparations and must therefore be con- 
sidered for the present at least in the light of histologic specu- 
lations. 

Diseases of the Pulp 

The pulp, because of the character of its blood supply, being 
devoid of collateral sources of nutrition ; because of the lack of 
adaptability of its vessels to changes in blood pressure; because 
of the character of its immediate surroundings, hard and un- 
yielding; because of the liability of its protecting tissues (the 
enamel, the dentin, and the cementum) to diseases which de- 
crease their thickness or density, and hence lessen their power 
to act as barriers against disease-producing influences, thermal, 
chemical and bacterial, — is susceptible in an exaggerated degree to 
diseases which in the vast majority of cases impair its vitality 
permanently. While from a pathologic standpoint the pulp is 
subject to a number of diseases, each of which will be discussed 
under its own heading, from the clinical standpoint diseases of 
the pulp are considered from two main aspects only. The group 
in which conservative measures can be successfully employed 
with the view of preserving the pulp, is one; and the group which 
demands as the only permanent compromise the sacrifice of the 
organ, is the other. 

In the first group is included, mainly, hyperemia, when it is 
a pathologic entity in itself and is nonbacterial in origin. In 



506 DENTAL PATHOLOGY 

the second group are included all diseases of bacterial origin, 
and those persistent forms of nonbacterial hyperemia which lead 
to nonseptic pulpitis and death of the organ. 

The pulp is also subject to retrograde as well as to construc- 
tive metamorphoses. In the former group are included the fibroid 
degenerations of Hopewell-Smith, and those presenting similar 
characteristics as described by Talbot, Latham, Wedl, Wahlkoff 
and Rothman; also fatty, hyaline and colloid degenerations, 
recognized only upon postmortem examinations of the pulp. 8 

In the latter group are included calcareous infiltration of the 
pulp, calcifications of the dentinal tubuli, pulp nodules and secon- 
dary dentin. 

General Predisposing Causes 

In the discussion of diseases of the pulp, the predisposing as 
well as the exciting causes should be considered. The predispos- 
ing causes may be general or local. Neither heredity nor sex are 
of any moment in this connection. Age is considered as a pre- 
disposing cause mainly because during childhood and, say, up 
to sixteen years, children do not take care of their teeth in a 
manner conducive to the prevention of caries, and consequently 
inflammation of the pulp is more frequent than later in life, 
when the development and progress of caries is prevented by 
hygienic care and filling operations. As the child grows the at- 
tacks of toothache from pulpitis and pericementitis become less 
frequent, but this should not be attributed to the influence of 
age itself. It is the result of conditions in which age plays no 
part whatsoever. Degenerations of the pulp are more frequent 
as age advances, and these degenerations "are not necessarily 
connected with the actual number of years of the individual's 
life, but with the age of the tooth and its pulp." Hopewell- 
Smith has found evidence of retrograde metamorphoses, such as 
fibroid degenerations, in children's deciduous teeth, identical to 
those degenerations incidental to old age. 4 

The amount and the composition of the blood varies in the 
presence of such systemic pathologic states as affect the lungs, 
heart, kidneys, spleen, pancreas, stomach, intestines, the blood, 
the lymph, the nervous system, etc., and these abnormal eondi- 

3Hopewell-Smith, A.: In N. G. Bennett's Science and Practice of Dental Surgery, 
New York, Wm. Wood & Co. 
-MIopewell-Smith, A.: Ibid. 



THE DENTAL PULP AND ITS DISEASES 507 

tions doubtless exert some influence upon the nutritional proc- 
esses in the pulp. The same must be said of diseases of me- 
tabolism, which become in time the precursors of chronic dis- 
eases in any of the viscera, and which leave their impress upon 
the pulp. In pyrexial and apyrexial maladies, degenerations 
(such as fatty or albuminous) of the pulp may occur. 5 

Anemia, chlorosis leukemia, may cause cell degenerations in the 
pulp. Gout, rheumatism, and allied conditions may lead to 
nodular deposits of calcified material in the pulp. 

Talbot's investigations go to show that changes in the blood 
current due to circulating poisons produce a deranged metabo- 
lism in the pulp which, by lowering its inherent resistance, ren- 
ders it liable to any of the several pulp diseases. 

Local Predisposing Causes 

Among the local predisposing causes Hopewell-Smith gives 
prominence to degenerative changes in the cells of the pulp, 
brought about by insufficiency of arterial blood supply and 
venous drainage, the result of constriction of the apical foramen 
or foramina. After the age of twenty-five he has found that a 
majority of teeth have apical foramina so diminutive that they 
must of necessity interfere with nutritional changes in the pulp 
and lead to certain types of degenerations. It is unquestionable 
that diminutiveness of apical foramina account not only for these 
degenerations, but also for the fact that the pulp has practically 
no power of repair, especially as the age of the tooth increases. 

The presence of metallic and of nonmetallic fillings must 
also be considered in the light of local predisposing causes, 
though to a less extent. A metallic mass in the tooth may lead 
to calcific degenerations within the pulp, these foreign calcified 
particles, acting as sources of irritation and by decreasing the 
resistance of the tissues, favor bacterial invasion from the ex- 
terior of the tooth, or via the blood stream. In the microscopic 
study of apparently healthy pulps the author has run across 
specimens showing small areas of chronic inflammation which 
must have existed for months, or perhaps years. The bacteria 
were evidently overcome to the extent of remaining in a semi- 



5 Hopewell-Smith, A.: Ibid. 
"Hopewell-Smith, A.: Ibid. 



508 DENTAL PATHOLOGY 

quiescent state for some time, causing very limited tissue de- 
struction and eventually their replacement by cells of an inferior 
organization. 

These facts are brought out to overcome the prevailing opinion 
that the pulp lacks in toto the power of overcoming infections, 
and to show that if a pulp be under constant stress by the pres- 
ence of calcific bodies within its substance, such a power of re- 
sistance to infection, be it ever so small, is rendered still more 
insignificant, or is completely abolished. Gysi has reported the 
regeneration of tissue in the pulp which has been destroyed by 
infection, but this tendency at the development of scar tissue in 
the pulp is very slight and rarely encountered. 

Exciting Causes: General 

Again, the exciting causes may be general or local. In the 
general are included changes in the quantity and quality of the 
blood as the result of chronic intoxications in any of the viscera, 
and of nervous disorders. These changes bring about cell de- 
generations in the pulp, which gradually impair its vitality and 
shorten its period of physiologic usefulness. The changes in the 
quantity and quality of the blood may bring about diseases of 
the vessel walls and changes in blood pressure. These changes 
in blood pressure, which affect the arteries throughout the body, 
must necessarily also leave their impress upon the vessels of the 
pulp. It is thus that we may explain the pulp hyperemia which 
develops in the course of febrile disturbances. The congestion of 
the pulp ceases upon the elimination of the causes responsible 
for the general rise in blood pressure. Here are instances in which 
nonbacterial agencies are the causative factors of pulp disease. 
Degenerations of the pulp, as the result of arteriosclerosis fol- 
lowing typhoid fever, septicemia, and other acute infections, have 
been described by Talbot who has also observed amyloid and 
hyaline degenerations within the pulp. 

Neoplasm of the pulp has been described by Latham. 7 It oc- 
curred in the pulp of an upper cuspid of a woman aged fifty-six 
giving a history of cancer in her family. Masses of cells were 
observed in the microscopical sections prepared from this pulp, 
which Latham interpreted as carcinomatous. 



^Latham, Vida A.: Neoplasm cf the Pulp, Jour. Am. Med. Assn., 1904. 



THE DENTAL PULP AND ITS DISEASES 509 

Exciting Causes: Local 

The local exciting causes are dental caries, erosion, abrasion, 
and any process by which the thickness or density of the enamel, 
dentin and cementum are decreased. In caries of the enamel, 
of the dentin, and of the cementum, in which bacteria have not 
gained access to the pulp, the pathologic manifestations in the 
pulp are the result mainly of thermal irritation, although chem- 
ical irritation also plays a part in the process. The same is the 
case with erosion and abrasion. The degenerations produced 
by these abnormal stimuli are constructive in character and mani- 
fest themselves in overcalcification of the dentinal tubules, cal- 
cific infiltrations of the pulp, and the formations of pulp nodules. 
The acid end products of carbohydrate fermentation- — the acid 
concentration being increased in the confines of the cavity — is a 
source of chemical irritation to the dental pulp, which may re- 
sult in degrees of stimulation leading to constructive degenera- 
tions; or when of greater intensity, to pulp inflammation ending 
in the death of the pulp. Bacteria which invade the pulp by way 
of a carious cavity are the most frequent exciting cause of inflam- 
matory disorders of the pulp. 



CHAPTER XL 

CALCIFIC DEGENERATIONS OF THE PULP AND OF THE 
DENTINAL TUBULL SECONDARY DENTIN 

Whenever the protecting tissues of the pulp suffer a decrease 
in thickness or in density the pulp becomes the seat of nutri- 
tional changes. The reason for this phenomenon is to be at- 
tributed to an increase in the intensity of thermal stimuli. The 
continued action of these abnormal stimuli results in an over- 
activity of the odontoblasts, or dentin-forming cells. The odon- 
toblasts so stimulated deposit, by means of the odontoblastic pro- 
longations, inorganic salts in the dentinal tubuli — tricalcium 
phosphate, mainly. The anatomic changes which thus result are 
an increase in the density and in the thickness of the walls of 
the tubuli, and possibly a decrease in the size of the dentinal 
fibrillar This process occurring in a number of tubuli results 
in an overcalcified area, the transparent zone of Tomes. It is 
the result, as previously stated, of odontoblastic stimulation, and 
is brought about by caries of the enamel; caries of the dentin; 
erosion; abrasion; metallic fillings; involuntary gritting of the 
teeth; violent brushing of the teeth; and by extremes of tem- 
perature, such as occur during a meal. Several theories have 
been advanced in explanation of dentin transparency, or the 
transparent zone of Tomes. Black 1 attributes this phenomenon 
to death of the dentinal fibrillas in the transparent zone (hyaline 
zone) from the irritation caused by the progress of caries. John 
Tomes, the first investigator to report upon dentin transparency, 
attributed it to a calcification of the dentinal fibrillae, or an in- 
filtration of the organic filaments by calcium salts. We consider 
it as the expression of a vital process — in fact the only view 
1 enable today. Miller 's experiments must be accepted as final, 
or at least so until such time as the weight of accumulated evi- 
dence to the contrary shall be forthcoming. The transparent 
zone is not observable in pulpless teeth, unless it be that the 
phenomenon occurred prior to the death of the pulp following 



Black: Operative Dentistry, Chicago, Medico-Dental Pub. Co., i. 

510 



CALCIFIC DEGENERATIONS 511 

infectious processes or accidental traumatisms, but occurs in 
teeth having live pulps following abnormal degrees of irritation 
brought about by the series of conditions above enumerated. 
Miller has reminded us that the opacity of dentin is the result 
of the difference in indices of refraction between the dentin ma- 
trix (the intertubular substance), and the dentinal tubules. There 
are two ways in which the transparency of an area of dentin may 
be brought about. In the one case it is by an increase in the 
amount of calcified substance within the tubuli, thus equalizing 
the coefficient of refraction between these and the dentin ma- 
trix ; or by decalcification of the dentin matrix, producing the 
same result. That decalcification of the dentin matrix does not 
occur has been shown by chemical analysis ; and as, in addition, 
a diminution in the caliber of the tubuli has been observed, the 
conclusion is forced upon us that it is a process characteristic 
of living dentin in which a degree of transparency is attained 
by the increase in calcified matter in the tubuli, which to some 
extent equalizes the coefficients of refraction of these and the 
dentin matrix. Miller observed the identical phenomenon in 
human senile teeth in which, doubtless, the pulps had been for 
many years subjected to mild degrees of irritation, in roots in 
the process of resorption, and in the abraded teeth of dogs. 

Secondary Dentin 

There occurs either in conjunction with the formation of the 
transparent zone, or at some subsequent time, or else independent 
of the transparent zone, the formation of additional dentin at 
the expense of the size of the pulp chamber and root canals (Figs. 
406-409). The secondary dentin so formed must be viewed in 
the light of a stimulation to the pulp of somewhat greater in- 
tensity than that which follows tubular calcification. Secondary 
dentin is classified as typical or amorphous, the typical variety 
being that in which the tubules in the newly formed dentin are 
more or less evenly distributed and resemble normal dentin. The 
amorphous is that in which the secondary calcification does not 
partake of the character of primary, normal tubular dentin. The 
forms of amorphous dentin have been classified by Hopewell- 
Smith as areolar dentin containing interglobular spaces; cellular 
dentin, in which the process of calcification has encapsulated 



512 



DENTAL PATHOLOGY 



some cells of the pulp; laminar, in which laminated masses of 
calcific matter appear; and hyaline, in which the calcific matter 




Fig. 406. — Secondary dentin. a, a, primary dentin; b, b, secondary dentin; c, c, pulp. 

has a smooth appearance. Secondary dentin may also occur 
through reflex action by reason of continued irritation in ad- 
jacent teeth. 



CALCIFIC DEGENERATIONS 



513 




Fig. 407. — Secondary 

dentin which entirely filled 
the pulp chamber, the 
original outlines of which 
can be distinguished from 
the secondary formation. 
Abrasion and erosion are 
responsible for the vol- 
uminous depositions of sec- 
ondary dentin. 



Fig. 408. — Secondary 
dentin in connection with 
abraded upper central. 



Fig. 409. — Secondary 
dentin in connection with 
severe abrasion. 




Fig. 410. — Pulp the seat of a chronic inflammation, a, an area of round-cell infiltration. 



514 



DENTAL PATHOLOGY 



Pulp Nodules 

Pulp nodules, or pulp stones, are amorphous masses of calcific 
matter found in the pulp chamber or in the root canals. It is 
the result of an activity of the pulp caused by direct or indirect 
abnormal stimulations. Pulp nodules, even though they give 
rise to no symptoms whatsoever during their deposition, and 
sometimes thereafter, must be regarded as the pathologic mani- 




Fig. 411. — Chronic inflammation of the pulp. The degeneration of the cells and fibers 
of the pulp results in the marked areolation seen in the specimen. 



festations of disturbed intrapulpal metabolism. The pulp nodule 
is more in the nature of a secretion within the pulp of the sub- 
stances entering into the composition of the nodule. In at least 
some cases it follows in the wake of chronic inflammation in 
limited areas of the pulp. The process of nodule formation is 
preceded by forms of cell degenerations— hyaline or fatty. In 



CALCIFIC DEGENERATIONS 



515 





Fig. 412. — Pulp stones occupying the Fig- 413. — Pulp stone (nodule) in pulp 

entire pulp chamber. chamber of lower molar, a. Tooth before 

splitting; b, and c, halves of the tooth with 
the pulp stone in situ. 





Fig. 414. — Pulp nodule filling up the 
entire pulp chamber. The nodule is not 
attached to the walls of the pulp chamber. 



Fig. 415. — A pulp nodule in siti 



516 



DENTAL PATHOLOGY 



l 




Fig. 416. — Decalcified section with pulp stone in situ, a, a, dentin; b, b, pulp stone it 

situ; c, pulp. 







Fig. 417. — Decalcified longitudinal section, showing a pulp stone in place. Notice 
the onion peel arrangement in the substance of the stone. It is not attached to the 
walls of the root canal, a, a, pulp; b, b, dentin; c, c, pulp stone in situ. 



8-7 
o Si 

3fl 



^S 







PJHP - 



^3 

CO IT 
rt- CO 

O 

3 2- 
n s 

CO 

> r 




is 

►1 •— • 
co'"* 


& 



ffk 



@ 



CALCIFIC DEGENERATIONS 517 

pulps studied by the author small areas of chronic inflammation 
have been found which had existed probably for months and 
years without giving rise to any symptoms whatsoever (Figs. 
410-411). It is therefore probable that those same areas become 
in some instances pulp nodules, following calcific infiltration. 
Fatty degeneration is responsible for the liberation of fatty acids 
which at first combine with the calcium brought to the degenerat- 
ing cells in the blood, the resulting calcium — fatty acid compound 
being decomposed into soluble phosphate or carbonate by the dis- 
placement of the fatty acids by phosphoric or carbonic acid. 
Pulp nodules do not resemble dentin —they are irregularly shaped 
masses ranging from such a size as to be visible under the mi- 



jjfc 



Fig. 420. — Pulp stones in pulp chamber of upper right first and second molars. 

croscope only, to a size to fill up the entire pulp chamber (Figs. 
412-420). The teeth in which pulp nodules exist may remain 
absolutely quiet and comfortable, and again may give rise to 
severe reflex manifestations in the shape of radiating neuralgia, 
the pain traveling in the direction of the ear, the eye, the tem- 
ples, and the back of the neck. 

Pulp nodules are found in the pulp chamber and in root canals. 
In these nodules occasionally calcospherites are found. In some 
instances the pulp contains in the root-canal portion a number 
of nodules which are accountable for the so-called lead-wire for- 
mation, as described by Black. Here also erosion and abrasion are 
frequently the cause of pulp nodules. The number and size of 
pulp nodules vary. In some microscopic sections examined by 
the author as many as fifty pulp stones were counted in one field 
of a pulp. 



CHAPTER XLI 

PULP HYPEREMIA 

General Considerations 

By pulp hyperemia is understood an abnormal condition in 
which the vessels of the pulp are engorged. The organ in most 
of the cases is the seat of active, rather than of passive, conges- 
tion, and responds to thermal stimuli with a degree of intensity 
more pronounced than is normal to it. The congestion is brought 
about either by paralysis of the vasoconstrictor nerves of the 
blood vessels of the pulp, or by stimulation of the vasodilators, 
following the infliction of degrees of irritation. G. V. Black 1 
was of the opinion that all pulp hyperemias are active or ar- 
terial, while Hopewell-Smith 2 argues that venous hyperemia of 
the pulp occurs more frequently than arterial. From the clinical 
standpoint this diversity of views has no significance whatsoever. 
Hyperemia proper is to be segregated from that hyperemia which 
is one of the phenomena of pulp inflammation, the former being 
considered here as a distention of the vessel Avails independent 
of any reaction to septic invasion (Figs. 421 and 422). It is 
practically in all instances of the active type; that is to say, the 
beginning is marked by changes in the caliber of the pulp arteries 
and in the quantity of blood which they hold. It must be noted, 
however, that as the result of a distention of the arteries and their 
increased blood contents there occurs a corresponding decrease 
in the lumen of the veins — a purely mechanical cause which we 
interpret as the inability of the veins to drain increased blood 
supply, because of their limited power of accommodation, limited 
as it is, to overcome exaggerated arterial pressure within the 
pulp. The pulp mass must continue constant on account of the 
unyielding character of its surroundings (the walls of the pulp 
chamber and root canals), so that a dilatation of one set of ves- 
sels — the arterial — must be synchronous with a compression of 
the other — the venous. 



M'.lack. G. V.: Special Dental Pathology, Chicago, Medico-Dental Pub. Co. 
2 lIopewell-Smith, A.: In X. ('.. Bennett's Science and Practice of Dental Surgery, 
New York, Win. Wood & Co. 

518 



PULP HYPEREMIA 



519 



Etiology 

The causes of pulp hyperemia are, indirectly, all disease 
processes or forces responsible for a decrease in either the thick- 
ness or density, or both, of the protecting* tissues of the pulp. The 
direct causes are the subjection of the pulp to stimuli of a de- 
gree of intensity greater than is normal for that pulp. In hy- 




Fig. 421. — Section of dental pulp, longitudinal. The distention and congestion of the 
vessels in the course of hyperemia is here beautifully shown. With the exception of the 
abnormal caliber of the vessels all the other tissue-elements are of normal appearance. 
a, a, a, a. distended vessels; b, b, odontoblastic laver. 



peremia of the pulp, the bacterial factor is excluded, except when 
indirectly induced by dental caries, when the destruction of 
portions of the enamel and of the dentin bring about irritation 
of the pulp by permitting the transmission of thermal impulses, 
which in the case of a sound tooth would not occur. Also 
it should be noted that the products of fermentation and putrefac- 



520 



DENTAL PATHOLOGY 



tion, especially when concentrated, act as irritants to the pulp, 
a condition which occurs constantly in a carious cavity. 

The pulp of each tooth, as pointed out years ago by Jack, has 
a temperature range peculiar to itself; a decrease of several 
degrees of temperature in this range, either from the higher or 
lower maximum, is to be interpreted as hyperemia. For instance, 
if a pulp, under normal conditions, does not respond to applica- 
tion of water of a temperature of from 98° down to 50° F., or 







-' m 






Fig. 422. — Cross section of hyperemic pulp. No pathologic lesion per sc is to be de- 
tected at this stage of the process. Some few distended blood vessels containing large 
numbers of blood cells are seen on the upper part of the picture, a, a, distended vessels. 

from 98° up to 128°, such a pulp has a temperature range of 
78°. This plan suggests the advisability in all cases in which the 
possibilities of hyperemia are brought into play (i.e. following 
the insertion of metallic fillings or the preparation of teeth for 
crowns), to obtain the temperature range before the hyperemic 
state develops. In the event of painful symptoms developing, by 
ascertaining whether or not a decrease in the temperature range 



PULP HYPEREMIA 521 

has occurred, a correct diagnosis can be more easily established, 
and the disturbed pulp is definitely located. 

The thickness or density, or both, of the protecting tissues of 
the pulp (enamel, dentin and cementum) are modified by disease 
processes as well as factors other than these. Among the former 
we include dental caries, erosion and abrasion ; among the latter, 
the removal by mechanical means of closely adjacent portions 
of the enamel or dentin preparatory to the restoration by crowns 
or fillings which have much higher degrees of thermal conduc- 
tivity (such filling materials as gold, or silver and its alloys). 
Furthermore, while per se the insertion of a small metallic filling 
may not perhaps cause hyperemia, the development of an exces- 
sive degree of heat in the process of polishing such a filling will 
frequently bring about this pathologic disturbance. Also the 
presence of a foreign mass, such as a filling of gold or of amal- 
gam, is in itself irritating to the dentinal fibrillar . 

Hyperemia or congestion of the pulp may also develop fol- 
lowing fractures of portions of the crowns of teeth, also follow- 
ing the traumatisms incident to the condensation of gold fillings. 
In the latter instance both the peridental membrane and the pulp 
may become affected. It may also occur from the action upon 
the pulp of chemical substances such as formalin, paraformalde- 
hyde, silver nitrate, zinc chloride, etc., and from the too rapid 
movement of teeth in orthodontia. 

The recovery from hyperemia depends upon a recovery of 
normal tone (contraction) by the vessels of the pulp, and is 
governed by the length of time the hyperemia has existed, the 
frequency and intensity of the paroxysms of pain, and the 
thoroughness with which the pulp environment is favorably 
changed. If the cause be a metallic filling, this should be re- 
moved and replaced by a filling of gutta-percha, and the use of 
foods or beverages of too low or too high a temperature must 
be most carefully avoided. In other words, the environmental 
disease-producing factors should be eliminated at once. 

Abrasion and erosion causing hyperemia, not infrequently neces- 
sitate the removal of the pulp if the disturbance is not promptly 
relieved by such methods as counterirritation or the use of co- 
agulant obtundents. In the absence of infection the pulp is capa- 
ble of fully recuperating from the effects of a hyperemia. Black 



522 DENTAL PATHOLOGY 

has shown that either moderate or relatively large liquid in- 
flammatory exudates are disposed of successfully by the pulp 
if placed under a nonirritating environment. 

The paroxysms of pain from pulp hyperemia may last from 
just a few seconds to several minutes, or hours, or even days. 
In some cases the pain is not exaggerated, although continuous ; 
in others it is both intense and continuous, — at times, for a period 
of seconds, the pain being unbearable. The pain may be lo- 
calized in the affected tooth, but may be felt in several teeth or 
in the entire side of the jaAV. It may also be of the radiating 
type, i.e. toward the temple, the ear, the eye, or the forehead. 
Occasionally a hyperemia in an upper tooth — the cuspid in par- 
ticular — will be reflected to all of the upper teeth posterior to it, 
and sometimes also to a number of teeth in the lower jaw of the 
corresponding side. An intense hyperemia with corresponding 
degree of pain, or a moderate hyperemia lasting for several 
Aveeks or months, if permitted to go untreated, ends in the death 
of the pulp; here the hyperemia has assumed the characteristics 
of a nonseptic pulpitis. All pain having ceased the patient feels 
greatly relieved both physically and mentally; but such a dead 
pulp may at any time give rise to an acute or a chronic alveolar 
abscess, and the chronic abscess may be either of the frank type 
with a sinus, or of the blind type without one. 



CHAPTER XLII 

GANGRENE OF THE PULP— PUTRESCENT PULP 

General Considerations 

By gangrene of the pulp (gangrenous decomposition) is meant 
death of the pulp en masse. It is the result of the shutting off 
of the circulation to the pulp through mechanical, thermal, or 
chemical factors, or as the result of paralysis of the vessel walls. 
The shutting off of the circulation at the apex may be caused 
by (1) blows upon the teeth, (2) tooth movement in orthodontia. 
(3) the -quick separation of teeth preparatory to filling opera- 
tions, or (4) nonseptic pulpitis leading to thrombosis and con- 
sequent infarction. The chemical causes are those incident to 
the application of so-called mummifying or tannifying sub- 
stances which contain formalin, tannic acid, thymol, zinc 
chloride, or other tannifying or coagulating substances. In 
the latter group of cases, the chemical substances used doubtless 
dehydrate the pulp, and by disturbing its metabolism to a de- 
gree beyond the possibility of cell recovery lead to cellular death 
(necrobiosis) of the pulp which, in the absence of bacteria and 
because of its complete dehydration, remains in the root canals 
as a shriveled mass. 

Paralysis of the vessel walls is caused by any form of shock, 
such as in a greater degree might cause the strangulation of the 
pulp at the apex. It is doubtful whether a pulp dies because of 
an actual strangulation (severance) of its blood vessels. Instead, 
it is more likely that the injury to the vessel walls is the cause 
of a thrombosis in either the arterial or venous trunk of the 
pulp. In other words, death of the pulp follows a series of 
arterial or venous obstructions, rather than a single strangula- 
tion. 

The. pulp which dies in bulk either remains in a state of dryness 
or mummification, or becomes infected. In the former condition 
all fluids in the pulp are absorbed and when the pulp-chamber is 
opened the pulp has a dried up, parchment-like appearance, 
with no offensive odor detectable. In the latter stage moist 
gangrene develops. 

523 



524 DENTAL PATHOLOGY 

By moist gangrene is meant putrefactive decomposition of the 
pulp, a process identical to that which occurs in the bodies of 
dead animals. The bacteria concerned in this process are sapro- 
phytes — bacteria which depend for their existence upon the prod- 
ucts of the decomposition of dead nitrogenous matter. It is, 
however, to be remembered that bacteria, even though parasitic, 
may, when circumstances demand it, develop saprophytic proper- 
ties. 

The organisms which have been found in putrescent pulps are 
both saprophytic and pathogenic, and it is more than probable 
that many forms are facultatively pathogenic and saprophytic. 
Long thread-forms, leptothrix, cocci, bacilli, spirillas and spi- 
rochetes have been found. Arkovy found the Bacillus gangrense 
pulpaB, the Staphylococcus pyogenes albus and aureus, the Strep- 
tococcus pyogenes and the Bacillus pyocyaneus. 

The breaking down of the tissue elements of the pulp is a 
process of simplification resulting ultimately in the formation of 
hydrogen sulphide, ammonium sulphide, carbon dioxide, and 
water. The albuminous substances are first changed into pep- 
tones; then such animal alkaloids as cadaverin, putrescin, and 
neuridin are formed; then nitrogenous bases such as leucin and 
tyrosin ; then aromatic products such as indol, phenol, and cresol ; 
and finally the simpler compounds H 2 S, C0 2 and H 2 0. 

In teeth the pulps of which are undergoing putrefactive decom- 
position, or a combination of suppuration and putrefaction, dis- 
coloration is liable to occur. In these cases the discoloration 1 is prob- 
ably due to a combination of factors, such as the formation of 
compounds of iron and sulphur (black ferrous sulphide); to the 
action of hydrogen sulphide (an end product of putrefaction) on 
hemoglobin, resulting in the production of sulphomethemoglobin ; 
and to the decomposition of hemoglobin, as already stated, in the 
case of unexposed pulps when the seat of nonseptic pulpitis. 

It has been argued that possibly the combination of ammonia 
(an end product of putrefactive decomposition, which in the 
presence of water is changed into ammonium hydroxide) with 
iron (liberated in the course of the decomposition of hemoglobin) 
is changed into Fe(OH 2 ), which upon being oxidized is changed 



*Kirk, E. C. : Discolored Teeth and Their Treatment, American Textbook of Opera- 
tive Dentistry, Philadelphia, Lea & Febiger. 



GANGRENE OF THE PULP 525 

into Fe 2 (OH) 6 , a reddish-brown compound. This may play a 
part in the discoloration of teeth whose pulps have under- 
gone putrefactive decomposition.* 

A tooth containing a pulp which is the seat of dry gangrene 
gives rise to no subjective symptom. The root canals are occupied 
by a mass of dried up tissues which, upon being exposed to the 
moisture and bacterial flora of the mouth, and to a liberal supply 
of oxygen (increased oxygen tension), usually precipitate within a 
short time an infectious apical pericementitis, either acute or 
chronic. 

Teeth in which the pulps have died following nonseptic causes 
become the seat of putrefactive changes in the presence of: 

1. Direct access to the pulp chamber (as through carious cav- 
ities, etc). 

2. Indirect access to the pulp chamber : 

(a) From under a defective filling. 

(b) From under a sound filling in a cavity from 
which all carious matter had not been removed. 

(c) From infected dentinal tubuli. 

(d) Through imperfections in the enamel. 

(e) Through cementum and dentin at the neck of 
the tooth following caries. 

3. By an infection which has reached the pulp via the circula- 
tion. 

Pulpitis 

Pulpitis, in a general way, may be defined as the aggregate 
of inflammatory phenomena in the dental pulp, which may be 
either bacterial or nonbacterial in origin ; it is distinguished from 
hyperemia in that the latter disease occurs in the absence of 
bacterial irritation and subsequent tissue destruction — two char- 
acteristic phenomena of pulpitis. This, of course, fails to hold 
good if the hyperemia is of such severity as to assume the charac- 
teristics of an inflammation. 

Nonseptic Pulpitis 

A nonseptic pulpitis is the result of subjecting the pulp to an 
exaggerated degree of the conditions responsible for the onset 
of hyperemia. An untreated hyperemia, in some instances, be- 

*Buckley, J. P. : Modern Dental Materia Medica, Therapeutics, and Pharmacology, 
Philadelphia, P. Blakiston's Son & Co. 



526 DENTAL PATHOLOGY 

comes a nonseptic pulpitis and ends in death of the pulp. The 
difference between nonseptic pulpitis and hyperemia, from the 
standpoint of pathologic anatomy, is that in nonseptic pulpitis 
occurs a diapedesis of leucocytes with, when very acute, a trans- 
migration of a few erythrocytes and a transudation of serum ; while 
in hyperemia diapedesis does not occur, although occasionally a 
small number of erythrocytes are forced through the vessel walls. 
In traumatic pulpitis the destruction of tissue by proteolysis 
does not occur. The pulp cells die following the shutting off of 
the circulation of the organ by thrombi, or by the products of 
cell degeneration, fat, cell fragments, etc. If the pulp remains 
free from bacteria the tooth will remain comfortable, usually 
until such time as an attempt is made to remove the dead con- 
tents of the root canal, when not infrequently a dentoalveolar 
abscess develops as the result of the passage through the apical 
foramen into the periapical tissues of the products of putrefac- 
tive decomposition and of bacteria; and also of a change in oxy- 
gen tension in the root canals. 

Septic Pulpitis 

The pulp is very susceptible to the effects of bacterial invasion, 
and being possessed of a minimum of recuperative powers, be- 
comes without delay the seat of a destructive inflammation upon 
being subjected to even the mildest degree of bacterial infection. 
The virulence and number of the bacteria and the degree of vital 
resistance of the tissues of the pulp determine whether the in- * 
fection will pursue a rapid course with proportionate rapid tissue 
destruction, or whether the course will be slow and the destruc- 
tion of the pulp will consume a longer period of time. Acute- 
ness and chronicity are differentiated from the standpoint of the 
duration of the inflammatory process up to the time of the death 
of the pulp. While determined clinically in most cases by the 
severity or mildness of the pain, together with the period of time 
the pain has been present, this symptom is not, however, in all 
cases, a true index of the degree of infection. In some cases in 
which death of the pulp occurs in a short time following an in- 
fection, the pain is neither severe nor paroxysmal, but rather 
mild and practically continuous, which, bearing in mind our 
clinical diagnosis, would be, as far as the degree of pain is con- 



GANGRENE OF THE PULP 527 

cerned, indicative of chronicity rather than of acnteness; and 
again, in other cases in which the infectious pulpitis is of long 
duration, the pain may be just as intense as that which accom- 
panies the severer infections, which once more would reverse the 
usual findings. 

In the presence of a wide opening by caries into the pulp cham- 
ber, even an acute process of pulp destruction may not give 
rise to extremely painful phenomena, since the inflammatory 
exudates find an outlet into the cavity of decay, so that the pres- 
sure within the pulp will at no time reach the maximum — unless 
it be when the exposure becomes obstructed with food debris. 
To the contrary, an inflammatory process by less virulent organ- 
isms in the pulp chamber or root canals, in the absence of drain- 
age, may give rise to very intense pain, as occurs when the open- 
ing into the pulp chamber through an unfilled cavity becomes 
clogged with food debris, or when a slowly progressive infectious 
pulpitis develops following the insertion of a filling. The pain 
factor is modified in accordance with conditions which favor or 
prevent maximum degrees of pressure. These must be borne in 
mind and looked to in making a diagnosis. Chronic infectious 
pulpitis is the exception rather than the rule. 

In pulps containing the products of suppuration in the shape 
of extravasated serum, liquefied pulp cells, and liquefied leu- 
cocytes, cells partially or completely disorganized, the reactions 
to cold applications decrease the existing pain, while the re- 
actions to heat applications are very marked. In the wake of 
the suppurating process a putrefying process may be following, 
and the gaseous end products expanding under heat increase the 
pressure against the peridental membrane in the apical area and 
against the medullary substances in the adjoining cancellated 
spaces. There is also a sense of pressure in the tooth and in the 
tissues overlying it. and pain, which varies in severity according 
to whether the inflammatory exudates remain enclosed in the 
root canals or are discharged through an exposure into a carious 
cavity. 

The infection of a pulp by pyogenic bacteria may occur in the 
complete absence of caries, the infection traveling in the peri- 
dental membrane, perhaps following a chain of epithelial rem- 
nants, or coming from the seat of septic apical pericementitis in 



528 DENTAL PATHOLOGY 

a neighboring tooth ; and again, a tooth which is the seat of 
chronic nonseptic pulpitis may become the seat of septic pulp- 
itis, when the evidence points to the entrance of bacteria into 
the pulp via the circulation. Dental caries may have progressed 
so far as to frankly expose the pulp; or the infection may ante- 
date the exposure, in which case the bacteria have penetrated 
through the dentinal tubuli into the pulp. In young teeth in 
which the diameter of the tubuli is relatively larger, the chances 
of infection of the pulp by the passage of bacteria through them 
is, of course, greater. But caries is not the only cause of 
pulpitis. In advanced pyorrhea the infectious process may reach 
the apical tissues and involve the pulp ; also a peridental infec- 
tion in a neighboring tooth may spread so as to involve the pulps 
of adjacent teeth. Pulpitis is characterized by changes in the 
dental pulp similar to changes which occur in other tissues of 
the body as the result of an infectious inflammation. Pulpitis 
may result in the complete disorganization of the pulp. 

In cases of pulp suppuration the tissue-cells, which have died 
consequent upon the action of the pyogenic bacteria and their 
toxines, may become the seat of putrefactive decomposition with 
manifestations identical to those which develop in the case of 
moist gangrene of the pulp. A pulp which has died following a 
traumatism or the action of chemical agents, in the absence of a 
direct or indirect exposure, may remain quiescent for a long time 
and then become the seat of putrefaction and its sequelae. 

Pathologic Anatomy 

FolloAving the presence in the pulp of bacterial exciters, the 
arteries at first contract for a very short time. This contraction 
is then followed by a dilatation affecting, in the order given, 
arteries, veins and then capillaries. The blood current is now 
temporarily accelerated, but by the time the dilatation of vessels 
is complete, this temporary acceleration is changed into a pro- 
gressive retardation. Leucocytes adhere to the vessel walls; the 
axial circulation becomes rich in red blood cells; leucocytes pass 
through the vessel walls (cliapedesis), and exudation of serum 
takes place. The toxines of the bacteria kill and liquefy the 
cells (Fig. 423) of the pulp, and these, together with dead and 
liquefied leucocytes, leucocytes in various stages of degeneration, 



GANGRENE OF THE PULP 



529 



fixed-tissue cells and serum exudate, constitute the pus found in 
a pulp chamber or root canal in which the pulp is succumbing 
to the effects of a pyogenic infection. 




Fig. 423. — Longitudinal section of a dental pulp, the upper portion of which has been 
the seat of a suppuration. The hazy area in the top of the picture represents cell 
liquefaction. Focusing did not change the appearance. 



The reparative power of the pulp being practically nil, the in- 
fectious process Avill advance uninterruptedly, in practically all 
cases, until the entire organ is destroyed. 



530 DENTAL PATHOLOGY 

The infection of the pulp may assume the ulcerative form or 
the circumscribed form — pulp abscess. In the former instance 
the pulp exhibits no tendency to circumscribe the infection 
which proceeds until the entire organ is destroyed, and may 
spread to involve the periapical tissues and give rise to an 
acute or chronic dentoalveolar abscess. In the latter instance a 
condensation of inflammatory cells (round-cell infiltration) takes 
place. A degree of resistance of the pulp almost equal to the 
degree of virulence of the infection is responsible for the suc- 
cessful efforts to partially ward off the infection. 

Clinically the pulp abscess and the uncircumscribed infection 
are not distinguishable. The symptoms may be equally severe 
in both conditions. 

The discoloration of a tooth Avhose pulp has not been exposed 
to bacterial influence through an opening in the pulp chamber 
(absence of caries), but has been the seat of an acute inflamma- 
tion leading to the formation of thrombi and emboli and to 
hemorrhagic infarcts, is due to the impregnation of the dental 
tubuli and dentin matrix with the products of the hemolysis of the 
erythrocytes in the extravasated blood serum. The tooth assumes 
at first a pinkish hue, which may be very light. In time, after 
going through a series of discolorations, such as yellow, brown, 
and slaty-gray, it may become even black, due to the progressive de- 
composition of the hemoglobin, forming methemoglobin (brown- 
ish red), hemin (bluish black), hematin (dark brown or bluish 
black), or hematoidin (orange), 2 either alone or in combinations. 

Pulp Hypertrophy- 
Pulp hypertrophy is the result of a combined bacterial and 
mechanical irritation. The pulp as a whole has been infected 
by bacteria of a low degree of virulence for a prolonged 
period of time. It is a chronic infectious process in the pulp. 
This slow inflammation results in the proliferation of fixed-tissue 
cells into masses of embiwonic (granulation) tissue. The enlarge- 
ment of the pulp continues as long as the degree of irritation per- 
sists. 



2 Kirk, K. C. : Discolored Teeth and Their Treatment, American Textbook of Opera- 
tive Dentistry, Philadelphia, Lea & Febiger. 



GANGRENE OF THE PULP 531 

To this bacterial irritation there may in time be added a me- 
chanical one, caused by the impingement of the enlarged pulp 
upon the edges of an exposure. The vascularity of an enlarged 
or hypertrophied pulp, and that of protruding gum tissue, is 
about equally active. The sensitiveness is variable, in some cases 
the enlargement being entirely devoid of nerve filaments. Sensi- 
tiveness in these cases is apparent only after removal of the bul- 
bous section of the pulp. 

Visible pulp hypertrophy can, of course, exist only in the pres- 
ence of an aperture leading into a cavity of caries. Black has 
described cases in which a hypertrophied pulp has been accom- 
panied by resorption of the dentin. The replacement of portions 
of the odontoblastic layer by giant cells has been observed in 
connection with chronic inflammations of the pulp. Perhaps 
these giant cells are present in conjunction with pulp hyper- 
trophy in those instances in which absorption of areas of dentin 
occurs. It may also be possible, as it has been recently observed 
in the case of bone resorption, that there takes place an infiltra- 
tion by leucocytes which assume osteoclastic functions and, 
through breaks in the odontoblastic layer, come into contact with 
the dentin, causing its resorption in limited areas. 

Occasionally these hypertrophic changes in the dental pulp 
are associated with calcareous formation; within the enlarged 
organ. The bulk of an enlarged or hypertrophied pulp is made 
up of granulation tissue which in time may change, all or a por- 
tion of it, into fibrous tissue. Occasionally the periphery of a 
hypertrophied pulp will present cellular elements resembling 
epithelial cells, the origin of which, if they are really epithelial 
cells, is certainly obscure. 



CHAPTER XLIII 

CYSTIC ODONTOMAS 
By G. B. New, M.B., Mayo Clinic, Rochester, Minn. 

.Cystic odontomas will be considered under two classes — the 
simple cysts and the adamantinomas. The single cysts are again 
divided into two types: Type A, including the cysts commonly 
called dental or root cysts; and Type B, those usually called 
follicular cysts, and containing a partially formed tooth. The 
term "follicular" cysts used for the second type is misleading 
in that one takes for granted, without knowing definitely, that 
this type is developed from the follicle of a tooth. The term 
"dentigerous" cyst is used quite loosely and may refer to either 
of the foregoing types of simple cysts. For this reason it has 
not been used in this classification. 

Twenty-six cystic odontomas are herein reported from the 
Mayo Clinic. Twelve of these are simple C} T sts of Type A; six 
are of Type B; and eight are adamantinomas. 

Simple Cysts of Type A 
The simple cysts (Type A) are the most common cysts of the 
jaws. Because of their little surgical importance, they have not 
received the attention which has been given to other cystic odon- 
tomas. Magitot, 1 in 1872, published the first important work on 
the subject of cystic odontomas, and attributed their origin to the 
development of the embryonic dental tissue. Malassez, 2 in 1885, 
found masses of cells about the roots of teeth in the jaws of 
adults and concluded that these were the remains of the dental 
ridge, the epithelial cord, and the outer layer of the enamel or- 
gan. These cells may be found near the teeth and are sometimes 
found deep in the jaws. Malassez called these masses of cells 
debris epitheliaux dentaircs, and proposed the theory that all cystic 
odontomas were derived from this group of cells. This theory 
is the one most commonly accepted. 



'Magitot: Arch. gen. de med., 1872, p. 339. 
2 Malassez: Arch, de physiol. norm, et path., 1885, p. 



129. 



CYSTIC ODONTOMAS 



533 



According to Scudder, 3 this type of cyst is found more com- 
monly in the upper jaw in the incisor and bicuspid regions. Of 
the twelve cysts of this series, six occurred in the upper jaw and 
six in the lower. Of those in the upper jaw four occurred in the 
incisor region, one in the bicuspid region, and in one case the lo- 
cation was not noted. In the lower jaw three occurred in the 
incisor region, two in the bicuspid region, and one in the molar 
region. 




Fig. 424. (New.) 

The t} T pical mammalian dentition consists of forty-four teeth; 
and man has but thirty-two, a third incisor, a third bicuspid and 
a fourth molar being missing. The most frequent location for the 
appearance of supernumerary teeth is in the upper jaw in the 
incisor and bicuspid regions. Whether these teeth are a rever- 
sion to the earlier types in the mammalian dentition, or simply 
mishappenings, is a questionable point among those who have 
made a thorough study of the subject. It is interesting to note 
that this type of cyst and the supernumerary teeth most fre- 

3 Scudder: Tumors of the Jaw, Philadelphia, W. B. Saunders Co., 1912. 



534 DENTAL PATHOLOGY 

quently occur in the same location, which might suggest that 
these cysts are derived. from supernumerary embryonic centers. 

The theory has been held for some time that these cysts develop 
from irritation or stimulation. The irritating factor may be the 
eruption of a tooth or some form of peridental inflammation. These 
cysts are frequently found in connection with the dead roots of 
teeth, and thus the irritative factor, necessary to stimulate their 
growth, is accounted for. 

Simple cysts of Type A occur at almost any age. Of the twelve 
cases reported in this chapter, the youngest patient was 12 years 
of age and the oldest, 70. The cyst is usually about the size of 
an English walnut, but may attain great dimensions, and in the 
upper jaw, simulate an empj^ema of the antrum. In the lower 
jaAv it may become as large as an orange. The cysts from our 
series varied in size from that of a cherry to that of a small 
lemon. Tumors the size of a pea and smaller, are occasionally 
found about extracted teeth. They were placed sometimes near 
to, and sometimes distant from, the root of the tooth. They con- 
tained fluid and had an epithelial lining indistinguishable from a 
larger cyst. The cysts have a smooth mucous membrane covering 
in the mouth; the wall varies in thickness and consists of a thin 
shell of bone (Fig. 424). 

Simple Cysts of Type B 

Malassez believes that this type of cysts also originates from 
cells that he describes in the jaws. Bland-Sutton, 4 however, be- 
lieves that this type simply represents an expanded tooth follicle. 

These cysts occur in either jaw with about equal frequency, 
and usually in the bicuspid and molar regions. 

Of the six cases in our clinic, three were found in the upper 
and three in the lower jaw. Of the three in the upper jaw, one 
occurred in the bicuspid region, one in the molar region, and in 
one case the location was not noted in the history. Of the three 
in the lower jaw, one occurred in the bicuspid region, one in the 
anterior part of the jaw and one in the molar region. 

This type of cysts occurs during or shortly after the second 
dentition — except those in connection with the third molar, which 
develop later in life. Although this fact is commonly known, this 



4 Bland-Sutton: Tumors, Innocent and Malignant, New York, Cassel & Co., 1901. 



CYSTIC ODONTOMAS 535 

type of cysts may not cause symptoms or be noticed until later 
in adult life. 

Of our cases, other than those in which the cyst occurred in 
the third-molar region, the ages of the patients were 3, 14 and 
28 years ; of those in the third-molar region, the ages were 27, 
34 and 37 years. 

It is noted that a tooth is missing from the set and a partially 
developed one is found in the cavity of the cyst. The crown of 
the tooth is usually complete and the root partially formed. These 
cysts occur about a partially developed permanent tooth and are 
rarely seen about a supernumerary tooth. 

In one of our cases the cyst occurred in a man 69 years of age. 
He had had a tumor of the lower jaw near the angle for forty- 
two years, and during the last six months it had increased in 
size and the surface had become ulcerated in the mouth. The 
roentgenogram showed a cyst with a partially developed molar 
tooth. A specimen from the cyst, on microscopic examination, 
proved it to be epithelioma. The extensiveness of the growth 
and the glandular involvement made the condition inoperable. 

This type of cyst has similar characteristics as to size as the 
cysts of Type A. The wall consists of thin bone and the mucous 
membrane covering in the mouth is quite smooth. 

Adamantinomas 

The adamantinomas, on account of their greater surgical im- 
portance and their interesting features pathologically, have given 
rise to more study than the other types of cysts. It has been held 
that, in the formation of enamel organs for the several teeth, 
there was a surplus of those formed and that these additional 
dental germs were the origin of the adamantinomas. Malassez' 
theory as to their development from the epithelial masses found in 
the jaws is accepted by most observers. Kruse agrees with Ma- 
lassez as to the origin of the cysts, and reports three cases, each 
one typifying different stages in the development of the cells of 
the enamel organs. Biichtemann and Kolaczek believe that these 
tumors originate from the mucous membrane or from the mucous 
glands of the mouth. Bland-Sutton and others hold that they 
are formed from the oral mucous membrane. Bland-Sutton's 
argument against Malassez' theory is that they occur in middle 



536 



DENTAL PATHOLOGY 



life and that if they were derived from the embryonic enamel 
organ, they would occur at an earlier period in life. 

The adamantinomas are most frequently seen in the lower jaw. 
Lewis 5 states that they are seen eleven times more frequently in 
the lower than in the upper jaw. The bulk of the tumor mass is 
usually at the angle of the jaw extending upward to the ramus 
and forward into the body of the jaw. Sometimes the entire 
ramus is cystic with the tumor extending across the mid-line to 
the other side of the jaw. These tumors may originate in the 
molar or bicuspid regions, but are rarely seen originating from 
about the anterior teeth (Figs. 425 and 426). 




Fig. 42. 



New.) 



I have been able to collect nine cases in which the tumor oc- 
curred in the upper jaAV, two from the Mayo Clinic. In only four 
of the cases reviewed in the literature were there definite data 
as to the location in the jaw. Four of the nine occurred in the 
posterior part of the jaw and two in the cuspid region. These 
cysts may originate close to the alveolar border or may start 
from deep within the jaw. Of the eight cases of adamantinomas 
from our clinic, six occurred in the lower jaw and two in the 
upper. Of the tumors in the lower jaw, in four the main mass 



5 Lewis: Surg., Gynec, and Obst., 1910, p. 28. 



CYSTIC ODONTOMAS 



537 



was located in the angle of the jaw, in one in the molar region, 
and in one in the bicuspid region. Of those in the upper jaw, 
one occurred well back in the molar region and one in the cuspid 
region. 

These cysts may develop at any age. Massin reports a case in 
a new born infant, and cases have been reported late in adult 
life. Lewis states that the average age of the patients in the 
seventy cases which he collected in the literature, was thirty- 




Fig. 426. — (237051. Roentgenogram of case in Fig. 425, showing entire absence of 
ramus of jaw on right side and the tumor extending across midline to bicuspid region 
on left side. (New.) 

three. The average age of the patients in our group of cases is 
twenty-seven and one-fourth years. Of the six cases from the 
literature, in which the tumor occurred in the upper jaw, the 
average age of the patients with occurrence in the molar region 
was thirty-three and one-half years,- and of those with occurrence 
in the cuspid region, sixteen and one-half years. 

Stumpf says that if either of the theories which have been ad- 
vanced for the etiology of the formation of these cysts is ac- 
cepted, one must assume some additional irritant factor as nee- 



538 DENTAL PATHOLOGY 

essary in their production. The lower molar region receives more 
irritation than any other locality in the month. It is an accepted 
fact that the lower third molar is more difficult to erupt and 
more frequently impacted than any other tooth in the mouth. 
It is interesting to note that it is in this region and at the 
average age of thirty-three years — during or just at the 
time of the eruption of the lower third molar — that these cysts 
occur. This suggests that the eruption of the teeth may play an 
important part in the chronic irritation which is probably neces- 
sary to stimulate the growth of these tumors. If these conditions 
develop from supernumerary embryonic centers the different lo- 
cations in the molar region may be explained by the fact that, 
according to Black, the supernumerary molar tooth may occur 
in any location posterior to the first molar. The adamantinomas 
are sometimes associated with cysts containing partially formed 
teeth, but not frequently enough to make this a factor in the 
etiology. 

It is difficult to obtain conclusive evidence of the association of 
the eruption and impaction of teeth to adamantinomas, as most 
histories are not of sufficient detail on this point. Two of the 
adamantinomas in our clinic were associated with unerupted 
third molars, one in the upper and one in the lower jaw. 

Of the seventy cases that Lewis collected from the literature, 
the average duration of symptoms was eight and one-half years. 
The duration of the symptoms in our cases was from ten months 
to twenty-one years. Most of the cases were of more than ten 
years' duration; but the exact duration of these tumors is diffi- 
cult to determine on account of the long standing of the condi- 
tion. 

None of the eases reported here had any glandular enlargement. 

These tumors present a smooth mucous membrane in the mouth 
unless they are infected. The walls of the cyst consist of a thin 
layer of bone. Crackling may be elicited in some areas, on pres- 
sure, where the bone is thin, and fluctuation may be found in 
others. These tumors may give rise to great pain when they are 
of large size because of pressure by enclosed fluid. One of our 
patients who had had a tumor for twenty-one years, for some 
years, in order to relieve the pain, tapped the cyst herself as 1 He 
fluid accumulated, by means of a sterilized hat-pin. 



CYSTIC ODONTOMAS 



539 



Pathologic Anatomy 

The lining of the simple cyst, Type A, consists of a layer of 
fibrous tissue and a thin layer of flattened epithelial cells. In the 
older cysts the latter layer may not be present, owing probably 
to the pressure from the enclosed fluid. Barrie, in 1905, reported 




Fig. 427. (New.) 



a case of dentigerons cyst which was probably a simple cyst, 
Type A, with typical adamantine epithelium, with no down- 
growth, lining the cyst. This was the first case reported with 
this type of epithelium forming the wall of the cyst. 






540 



DENTAL PATHOLOGY 



The lining- of the simple cyst, Type B, consists of a fibrous tis- 
sue layer. Some observers have reported an epithelial lining for 
this type of cyst also. 

The adamantinomas, on section, present solid and cystic areas. 
The cystic areas vary in size from that of the head of a pin to 
that of an English walnut. They appear to have a smooth lining. 




Fig. 428. (New.) 



and fibrous or bony septa are seen separating the various cysts. 
The cysts contain a lli'ni yellowish fluid. The solid areas have a 
red tint and present a granular appearance, owing to the many 
minute cysts. 

Microscopically, the solid areas consist of a fibrous tissue 
stroma and columns of epithelial cells. These columns may be 
elongated, rounded, or arranged in the form of acini, and may 
present many irregular forms. Two types of epithelial cells are 



CYSTIC ODONTOMAS 



541 




Fig. 429. (New.) 




Fig. 430. (New.) 



HB^HUHHMiH^B^n 



542 



DENTAL PATHOLOGY 



found in these cell columns: the typical columnar cells with the 
nucleus placed near the pole away from the stroma; and the 




Fig. 431. (New.) 




Fig. 432. (New.) 



differentia ted cells from this type — the polygonal cell and a stel- 
late cell, which form the main mass of the epithelial columns. 



CYSTIC ODONTOMAS 543 

These cells are analogous to the cells that form the enamel organ. 
Areas of transitional forms from the solid cores to the small 
c}^sts are seen. The stellate cells are seen undergoing disinte- 
gration, their places being taken by cyst-cavities, at first quite 
small and then becoming larger. Stellate cells gradually dis- 
appear and are replaced by the fluid of the cyst. As the cyst in- 
creases in size, the columnar cells are alone left to line the cyst, 
while in the yet larger cysts these have disappeared and the Avail 
consists of fibrous tissue only (Figs. 427-432). 

The diagnosis of the cystic odontomas, when the facts already 
noted are considered and with the aid of the roentgenogram, is 
usually not difficult. The roentgenogram will sIioav a partially 
developed tooth, a unilocular cyst, or the septa in the multilocu- 
lar variety. The differential diagnosis from a giant-cell sarcoma 
is usually the most difficult, and this has frequently to be made 
at the time of operation or by microscopic examination. 



CHAPTER XLIV 

MOUTH INFECTIONS IN THEIR RELATION TO SYSTEMIC 

DISEASE 

"While among the thinking practitioners of medicine and den- 
tistry the relation of mouth infections to systemic disease had 
been surmised for many decades past, it is only within recent 
years that the subject has been given proper scientific attention 
by investigators in both professions. The investigations of the 
late Miller, a pioneer in this as in other fields of dental pathology, 
of Kirk, Hartzell, Henrici, Moorehead, Price, Rosenow, Billings, 
the Mayos, A. D. Black, and of the present writer in collabo- 
ration with J. D. McCoy and C. C. Browning, constitute the source 
from which has been abstracted and systematized much of the 
information contained in this chapter. Hartzell, in 1908, pub- 
lished the result of his observations on the relationship of peri- 
apical infections to joint inflammations, in which he records the 
improvement of the systemic condition following the eradication 
by root amputations of the infections in the jaws. William Hun- 
ter, following personal observations for a period of years, called 
the attention of both professions to the significance of oral sepsis 
as an etiologic factor of many systemic disorders. 

The mouth, because it is exposed at all times to external influ- 
ence, and because it affords all the elements necessary for the 
growth and multiplication of bacteria, contains in both health 
and disease myriads of microorganisms which are carried into 
the deeper structures by the blood or lymph, there to propagate 
the moment the resistance of the individual or of some localized 
area of tissue anywhere in the body, descends below the normal 
for that individual. 

In order to have a clear understanding of the pathologic phe- 
nomena involved in the transportation of bacteria and bacterial 
toxins from the teeth to remote areas of the body, a careful 
study of the histology and anatomy of the investing tissues of 
the teeth and of the osseous substance of the jaws is the sine qua 
non. Nothing else will convey a clearer and more definite idea 

544 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 



545 



of the reasons why infections about the roots of the teeth can, 
under no circumstances, be considered as strictly localized proc- 
esses. 

The blood supply of the peridental membrane and that 
of the surrounding alveolar structures are not separate and inde- 
pendent vascular areas. The vessels anastomose freely among 
themselves. An infection located about the apex of a root pro- 
ceeds until the cancellated substance becomes involved. The 
cortical laver of bone lining' the alveolus soon breaks down as the 




Fig. 433. — Portion of a mandible with cortical layer of hone removed. The relation 
of the roots of the teeth to the cancellated substance of the jaw is seen. The abundance 
of blood vessels in the cancellated substance is responsible in some cases for the arrest- 
ment of the infection, while in fortunately infrequent instances it is the reason for 
severe metastases. 

result of the infectious processes which develop in the peri- 
apical space, and when this cortical layer disintegrates the in- 
fection at once reaches the cancellated bone of the alveolar proc- 
ess, which is a continuation of the cancellated spaces of the jaw 
proper (Figs. 433, 434, and 435). These spaces contain the 
medullary substance — a tissue richly supplied with blood vessels 
and lymphatics. The involvement of the alveolar walls is in the 
nature of a septic osteomyelitis. The medullary substance con- 
tained in the cancellated spaces becomes the seat of a chronic in- 



^HHBBBH 



546 



DENTAL PATHOLOGY 







Fig. 434. — Vertical gross section of mandible in molar region. An abscess which 
develops in the peridental membrane of the apical region soon involves this cancellated 
substance in which blood-vessels are numerous (in the myeloid substance). Acute or 
chronic osteomyelitis and metastatic infections are the probable results. 



■ 






IS 












• 








► 






& 









Fig. 435. — Decalcified transverse section of upper central incisors slightly above the 
alveolar crest with intervening alveolar process in situ. Following an infection of the 
peridental membrane beginning at the gingiva the alveolar bone becomes involved and 
results in a chronic osteomyelitis. 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 547 

flammation in which osteoclasts play an active part. Through 
osteoclastic action the hard substance of the bone disappears, 
the cancellated spaces are eaten through, and Haversian canals 
are widened. The contents of the spaces become the seat of a 
typical chronic inflammation containing large masses of small round 
cells. The bone lamella? are successively destroyed and carried away 
by osteoclasts, and in time the inflamed medullary substance also 
breaks down. In some places the cortical layer is less than one- 
third of a millimeter in thickness, and consequently it is quickly 
broken down, thereby opening up an abundance of avenues for 
the absorption of bacteria and bacterial toxins. An acute or 
chronic apical infection is practically at no time a localized in- 
fection. If all chronic infections about the roots of teeth do not 
give rise to systemic manifestations, it is not because the bacteria 
and toxins concerned in the infection are not in all cases at the 
portals of absorption, but rather because individuals are fre- 
quently able to ward off successfully a bacterial invasion. 

By the hematogenic and lymphogenic routes bacteria invade 
the viscera, muscles, joints and nerve structures, and there give 
rise to any one of a series of pathologic manifestations. It may 
be a gastric or duodenal ulcer, or an arthritis, or a myositis, or 
a neuritis. But it is not only through the hematogenic and lympho- 
genic routes that systemic manifestations of mouth infections 
develop. In suppurative diseases of the investing tissues of the 
teeth (pyorrhea alveolaris) in which pus is constantly discharged 
into the mouth, systemic involvement follows by a combination 
of (1) absorption by the blood and lymphatic capillaries of the 
gum and peridental membrane, and (2) by absorption through the 
gastric and enteric mucous membrane following the passage of the 
pyogenic discharges into the stomach. These discharges are con- 
veyed in the saliva, which is constantly swalloAved, and in the 
food. 

It has been shown by Metchnikoff that the blood obtained from 
animals after eating, contains bacteria, while blood from animals 
after fasting is sterile. Miller showed some twenty-five years 
ago that microorganisms swallowed in the food and saliva are 
not all destroyed by the gastric juice, estimating that eight out 
of every twenty-five bacteria swallowed are unharmed by the 



548 DENTAL PATHOLOGY 

gastric juice. C. H. Mayo, 1 relying on Smithies' observations, 
refers to a series of over two thousand patients with gastric dis- 
orders, in 87 per cent of whom bacteria were found in the stomach 
contents. Smithies found that "morphologically, cocci and diplo- 
cocci were present in 83 per cent; short and long rods (often of 
the colon group) in 58 per cent; typical streptococci and staphy- 
lococci in 17 per cent; and leptothrix buccalis in 24 per cent. In 
fifty-four cultural studies of the saliva from "dyspeptic" pa- 
tients, streptococci and staphylococci were demonstrated in over 
80 per cent, bacilli in 66 per cent, and leptothrix buccalis in more 
than 14 per cent. Comparing these figures, it would appear that 
the common forms of pus-producing organisms (streptococci and 
staphylococci) have their proliferation retarded in gastric juice 
but that bacilli (often of the colon group), as well as leptothrix 
buccalis, thrive in the stomach. 2 

It stands to reason that gastric mucous membrane weakened 
by disorders due to a gastric secretion unsuitable in quantity or 
quality, or both; by excesses in eating or drinking, or both; by 
the retention of undigested food which soon undergoes putre- 
factive changes; or by any other cause — must lose, to some ex- 
tent at least, its normal resistance to bacterial influences. Such 
being the case, a proportion of the ingested bacteria are bound 
to incite both local disorders and (with their entrance into the 
capillary and lymph vessels) inflammatory disorders in any of 
the body organs or tissues in which resistance to infection had 
been previously lowered, and into which the bacteria are carried 
in the blood or lymph streams. 

Oral foci of infection are not the only ones responsible for the 
development of chronic maladies; but when present, the problem 
of correcting these systemic disorders must also aim at the elim- 
ination of the oral foci, regardless of any foci located elsewhere 
in the body. The pendulum, it is claimed, has been made to 
swing perhaps too far in the direction of radicalism ; in former 
times, however, either through ignorance or caution, it had been 
held too far in the direction of conservatism. It may be that its 
having reached what some frankly decry as radicalism, has out- 
lined a safe middle ground for future practice. In that event its 



x Mayo, C. II.: Jour. Am. Med. Assn. 
2 Mayo, C. II.: Jour. Am. Med. Assn. 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 549 

service has been infinite. In the meantime this extreme swing- 
ing is helping innumerable victims of empirical dental methods 
of procedure to discard the yoke of invalidism, and to regain 
their respective places among the useful units of their communi- 
ties. 

Chronic mouth infection — oral focal infections — for the pur- 
pose of convenience in description we have divided into two 
groups; (1) the intraosseous and (2) the extraosseous. And be 
it understood that by "oral focal infection" we imply an area 
of chronic infection in the mouth — the teeth and its osseous and 
soft investing tissues — from which, through hematogenic or 
lymphogenic metastases, chronic disease develops in any organ 
or structure of the body at remote distance from the original 
focus of infection. 

In the intraosseous group are included the chronic and subacute 
infections in the substance of the jaws immediately adjacent to 
the roots of the teeth. These are consequent upon a chronic in- 
fection of the periapical peridental membrane — the sinusless 
chronic dento alveolar abscess (so-called dental granuloma) — to- 
gether with the secondary foci of infection arising from this 
rource. In the extraosseous group are included all chronic sup- 
purative diseases of the peridental membrane, alveolar process, 
gingiva and gums. 

In most cases of dental disease in which extensive destruction 
of the hard tissues of the tooth has taken place through caries, 
with involvement of the pulp as the consequence, a focus of 
chronic infection, if present, will, of course, be located in the 
deeper osseous structures of the jaw. These seats of chronic in- 
fection, the existence of which has not altogether been unknown in 
the past, have by some been designated as blind abscesses, by 
others, the author included, sinusless chronic dentoalveolar ab- 
scesses, and by still others denial granulomas. They play a very 
active part in the etiology of chronic inflammatory disorders in 
articular structures, muscles, heart, kidney, intestines, etc. In 
discussing foci of infection in the mouth we are prone to give the 
preference to these septic nuclei in the deeper structures of the 
jaw (rarefying osteitis). It is not our aim to minimize their im- 
portance; nevertheless, we feel constrained to state that these are 
not by any means the only dental or oral sources of general in- 



550 DENTAL PATHOLOGY 

volvement. It has been satisfactorily shown, however, that infec- 
tion of joints, muscles, the intestinal tract, kidneys, heart, etc., 
may take place via the hematogenic or lymphogenic routes. 

In the mouth are to be found numerous conditions which make 
possible the absorption of bacteria and their toxins directly into 
the circulation, in the absence of "blind abscesses"— namely, in 
the absence of chronic, acute or subacute pericemental infections. 
These extraosseous sources of toxin absorption are, in patho- 
logic significance, equal to, if not greater than, the intraosseous 
focal areas. The presence upon the surfaces of the teeth of sali- 
vary calculi which maintain the margins of the gum in a state of 
constant irritation, either through pressure atrophy or through in- 
duction of a suppurative process, cause the destruction of the 
stratified squamous epithelium protective covering, and constitute 
a prolific source of absorption of bacteria — and bacterial toxins. 
Almost invariably, when salivary calculi are present in varied 
amounts, such absorptions are going on constantly, not only from 
the locations in which the calculi are present, but also from ad- 
jacent areas which become involved by a process of continuity. Sal- 
ivary calculi exert a detrimental influence upon soft tissues and 
favor their invasion by bacteria. They also act mechanically by 
favoring the lodgment of food particles which, after undergoing 
fermentation or putrefaction, or both, give rise to either acid or 
alkaline end-products, which irritate the soft tissues and prepare 
the field for bacterial invasion by decreasing its vital resistance. 
Salivary calculi as a source of bacterial and toxin absorption, with 
possibly future systemic involvement, can not be too strongly 
emphasized. 

The other forms of calcareous deposits upon the teeth, namely, 
those deposits Which exist under the free margin of the gums, and 
which are brought about by some form of irritation of the gingival 
and septal tissues, eventually lead to the destruction of the peri- 
dental membrane and alveolus, and likewise constitute a frequent 
source of absorption of bacteria and bacterial toxins. Any form 
of injury to the gingivae, such as the rough edges of crowns and 
fillings; negligence in the care of the mouth permitting the accu- 
mulation of food particles which undergo decomposition and main- 
tain the gingival tissues in a state of constant irritation ; the pres- 
ence of unfilled cavities of decay; defectively contoured fillings; 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 551 

natural or acquired insufficiency of approxinial contact ; and other 
allied abnormal phenomena, are all important causative factors in 
this variety of deposits. Subgingival deposits invariably spell in- 
flammation of gum tissue and eventually the formation of pyor- 
rhea pockets. The gingiva, the peridental membrane, and the al- 
veolar process become the seat of a chronic infection; the peri- 
dental membrane and the overlying alveolar process become the 
seat of a destructive suppurative inflammation, slow in its develop- 
ment but, nevertheless, one which continues and in time will lead 
to the establishment of the pathologic condition which is ordinarily 
designated as pyorrhea alveolaris. 

The importance of the study of these conditions is made more 
understandable by recalling the list of maladies which clinical ob- 
servation has shown to be related in etiology to infections about 
the roots of teeth and their investing and supporting structures. 
The list includes endocarditis, myocarditis, pericarditis, joint and 
muscle infections, gastric, intestinal, renal and pulmonary infec- 
tions, toxemias, insomnia, sinus infections which become secondary 
foci, etc. 

Hartzell and Henrici have produced lesions of the heart, kidneys, 
aorta, and joints of rabbits following intravenous injections of 
8 c.c. of a twenty-four-hour broth culture of the strains of strepto- 
cocci obtained from pyorrhea alveolaris and dentoalveolar abscess. 

The mouth and teeth, the air sinuses, the tonsils, the postpharyn- 
geal adenoid tissue, upon becoming the seat of chronic infections, 
constitute jointly the most common forms of focal infection. From 
chronic dentoalveolar abscesses and pyorrhea alveolaris have been 
obtained different strains of streptococci — the hemolyticus, rheu- 
maticus, and viridans; also the Staphylococcus pyogenes albus and 
aureus, the fusiform bacillus, and the diplococcus of pneumonia; 
and from the saliva and pharyngeal mucus, in addition to the 
above are found the B. diphtheria, the B. tuberculosis, the M. 
catarrhalis, and a large number of saprophytic organisms. Any 
one of these pathogenic organisms may migrate into any struc- 
ture of the bod,y, as previously stated, by the hematogenic and 
lymphogenic routes, and finding areas of decreased vital resist- 
ance, start on their campaign of slow destruction. 

The Streptococcus viridans may occasionally produce acute in- 
fections even though the organism is one of low virulence and 



■■ 



552 DENTAL PATHOLOGY 

brings about chronic rather than acute inflammations. Acute 
joint inflammations have, however, been observed in which the 
Streptococcus viridans was the principal organism. 

We now direct the reader's attention to the advisability of 
disregarding the absence of subjective and objective symptoms 
in the diagnosis of mouth infections, having become long ago 
convinced that some of the most pronounced cases of systemic 
involvement had developed in cases in which there were to be 
found in the mouth no indications of the existence of a chronic 
inflammatory process. 

In the course of an investigation by James D. McCoy, a series 
of about 125 cases Avas radiographed, several extra- and intra- 
oral exposures being made of each case, making a total of nearly 
500 radiograms. In this series the radiograms showed, in each 
instance, some theretofore unsuspected pathologic condition, such 
as impacted and incarcerated teeth, incompletely filled root 
canals, foci of chronic infections, etc. Of the cases exhibiting 
chronic foci of infection (in each instance the condition being 
Unsuspected by the patient) a proportion of somewhat over 50 
per cent had systemic manifestations in the form of arthritis or 
myositis of various degrees of intensity. 

A clinical investigation covering a series of 125 cases con- 
stitutes a strong enough nucleus of data from which to deduct 
conclusions which should lead to a more definite conception of 
the role played by mouth infections in the development of joint 
and muscle inflammation. The fact that the existence of these 
mouth lesions had not been suspected at any time prior to the 
radiographic examinations, because of absence of subjective and 
objective symptoms, is the conclusion in McCoy's work which 
constitutes a strong link in the chain of evidence on the rela- 
tionship of mouth infections to systemic infections. 

The Streptococcus viridans, an organism of low virulence, has 
been obtained by Eartzell and Ilenrici from chronic clentoalveolar 
abscesses, and the same investigators 3 have obtained from 
one case of pyorrhea alveolar is and dentoalveolar abscess various 
strains of streptococci, the Staphylococcus albus, Bacillus coli, 
Bacillus proteus, various spore-bearing aerobes of the Bacillus 
subtilis type, and Bacillus pyocyaneus; also a small Gram-positive 



Jour. Am. Med. Assn , xliv, No. 13. 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 553 

bacillus and a diphtheroid bacillus. From another case they ob- 
tained a pure culture of Bacillus fecalis alcaligenes. 

Urlich made an examination of 1350 teeth, 82 per cent of which 
showed apical abscesses. He examined 976 artificially devitalized 
teeth with root canal fillings, and of these over 68 per cent 
showed apical abscesses. A bacterial examination was made in. 
318 cases and the Streptococcus viridans and the Streptococcus 
hemolyticus were found 309 times, or in 97 per cent of all cases 
examined. 

In nine cases of acute arthritis reported by Hartzell and Hen- 
rici in one series, the patients showed marked improvement im- 
mediately after the removal of the abscessed teeth. 

In another report they mention the case of a patient with pyor- 
rhea alveolaris, apical abscess and a severely painful arthritis 
which began to recede a few hours after the extraction of the 
tooth having the chronic dentoalveolar abscesses. Cultures from 
the root tip yielded another strain of streptococcus of high viru- 
lence, killing a rabbit overnight. This rabbit showed a hemor- 
rhage into one of the mitral cusps and a number of whitish 
streaks in the myocardium just beneath the pericardium. In 
these streaks were found, microscopically, the lymphocytes 
gathered together in the cellular tissues under the pericardium. 
The streptococci were recovered in pure culture and immediately 
injected in a smaller dose in another rabbit which died in two 
days; the only lesions obtained in this rabbit were numerous mil- 
iary abscesses in the kidneys, especially the medulla — a case of 
true pyemia. 

Hartzell and Henrici 4 have also studied seven cases of endo- 
carditis. In two of these patients the heart condition was vastly 
improved by eliminating the mouth infection. 

One from among the many observations on the relation of local 
dental infections to arthritis has recently been reported by 
Morej^. 5 In a series of six cases of arthritis of long standing, 
the symptoms subsided immediately upon, or a short time fol- 
lowing, the eradication of intraoral foci of infection, the sup- 
position being that the mouth streptococcus had been carried 
by the hematogenic route to the points of activity in the articu- 



4 rTartzell and Henrici: Jour. National Dental Association, vi, Xo. 12. 
r AIorey, F. L. : Acting Assistant Dental Surgeon U. S. Navy, in the U. S. Naval 
Medical Bulletin. 



554 DENTAL PATHOLOGY 

lations. No attempt is made by the reporter to connect all 
cases of arthritis with diseased teeth ; but, on the other hand, he 
brings forth additional and convincing proof that a large num- 
ber of cases of arthritis, nephritis, cardiovascular diseases, 
and inflammations in the gastrointestinal tract, are of dental 
etiology. 

Three cases in which infectious arthritis were cured by the 
removal of teeth having a slight area of infection are reported 

by Morey: 

Case 1 

Arthritis of the right ankle. Patient unable to bear any weight on 
his foot for about six. months; he had been under treatment most of the 
time but had not improved very much. A roentgenogram showed a slight 
area of infection above the right first molar, which had only a small occlusal 
amalgam filling in it; the patient was advised to have the filling removed and 
the canals treated, but he preferred to have the tooth extracted. Within two 
hours after the extraction the pain in the ankle began to subside and the next 
day he was able to bear his weight on the foot. 

Case 2 
Arthritis of the arms and legs, patient having been in bed for four 
months, some days feeling slightly improved but gradually growing weaker. 
No focus of infection could be found; a roentgenogram of the teeth showed 
a slightly infected area at the root of one of the molars. The first molars had 
gold crowns on them and it was thought advisable to remove the teeth that 
were crowned, as the patient was confined to his bed and it was impossible to 
open the teeth and treat the roots with any degree of satisfaction. Within 
five weeks after the extraction the patient was able to walk around, being free 
from all pain, and the swelling had disappeared. 

Case 3 

Confined to his bed with arthritis of the knees and ankles. Eemoved 
the left superior -first molar, it having a slight infection above it; also 
removed a badly broken-down root which was the source of some infection. 
Patient began to improve within forty-eight hours. 

Relatively small areas of rarefaction on the roots of teeth con- 
sequent upon chronic peridental infection are frequently the 
cause of severe joint infection. In some cases one single slight 
area of infection, upon its elimination, has brought about re- 
covery of the case. 

Hartzell and Henrici G report that in the study of a series of 
seventeen cases of arthritis deformans over one-half of these 
patients showed improvement, which in a few cases was pro- 

'"ITartzell, Thomas B., and ITenrici, Arthur T. : A Study of Streptococci from Pyor- 
rhea Alveolaris and from Apical Abscesses, Jour. Am. Med. Assn, xliv, No. 13. 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 



555 



nounced; other cases, however, became worse under treatment. 
In a series of seven cases of endocarditis, in two of the patients 
the heart condition was vastly improved. Other systemic dis- 
turbances studied by them were three cases of pernicious anemia, 
five cases of gastric ulcer, and nine cases of active arthritis. In 
the pernicious anemia cases no definite report was made by the 
investigators, although they state that one man showed a marked 
progressive increase in the blood count after removal of some 
of the abscessed teeth, but that he left the hospital before his 
dental work was completed, and returned later with a low blood 
count. The gastric ulcer patients, two of whom had been affected 
twelve to fourteen years with frequent recurrences in that time, 




Fig. 436.— Case 1. 

had no recurrence, since eliminating the mouth infections, dur- 
ing a period of observation of two years and five months after 
the dental work was completed. The arthritis patients all showed 
a marked improvement beginning in some cases a few hours 
after removing the abscessed teeth. 

The following reports of cases studied by the author from a 
series of several hundred will throw some light on the role of 
mouth infections as sources of systemic intoxications. 

Case 1 (Fig. 436) 
Woman, aged thirty-six, had previously been in apparent good health but 
complained of severe pain in her face. In addition, she complained of a series 
of symptoms typical of general toxemia. She seemed anemic and decidedly 



556 



DENTAL PATHOLOGY 



below par. She sought the services of a dentist for the purpose of ascertain- 
ing- whether any abnormality could be detected in her teeth that would ac- 
count for the reflex pain from which she had been suffering for some time past. 
An area of rarefying osteitis was found around the root of the second lower 
bicuspid, indicative of chronic sepsis in the peridental tissues and within the 
bony structures. The tooth had been previously treated and the root canal 
carefully filled. The bicuspid was extracted and almost immediately the pain 
and toxic symptoms began to improve, and have continued so uninterruptedly 
ever since. 

Case 2 (Fig. 437) 
Man aged forty-five gave a history of continued good health up to the time 
of the incidence of the symptoms which led to his being placed under our 
observation. He had evidently been a man of vigorous constitution and non- 
sedentary in his habits. He complained of loss of appetite, lassitude, and an 
inability to exert himself to any extent without experiencing a sense of fatigue. 




Fig. 437.— Case 2. 



The radiogram (Fig. 437) showed a marked chronic septic condition under the 
roots of the lower second molar, which evidently had been treated years pre- 
viously and in which the root canal had not been completely filled. There was a 
tenderness to percussion in several teeth and consequently a definite diagnosis 
could not be made at the time. The radiogram came to our assistance, the 
offending tooth was extracted, and a complete recovery followed within a 
period of three or four weeks. 

Case 3 (Fig. 438) 

Man, aged about sixty years. This case seems to us to present features of 
special interest because the septic conditions about the roots of some of the 
teeth were evidently responsible for an interruption in the mental balance of 
the patient. The man, of limited means, had endeavored for some time past 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 



557 



to secure a berth in an old man's home, but on account of the mental and 
physical symptoms the authorities of the institution rejected his application. 
He was referred by his physician to ascertain whether any abnormality could 
exist in his jaws and around his teeth which could be made to account for 
the toxic symptoms from which he was suffering and also for the disturbance 
in psychic function. We found that which would warrant one in assuming 
that the foci of infection in his jaws were at least a factor in the production 
of the pathologic symptoms herein described. On the left side conditions 
were as follows: 

A chronic abscess around the roots of the lower first bicuspid; an incar- 
cerated root in the upper jaw mesial to the second molar; also foci of in- 
fection in the distal root of the lower third molar, above and around the 
roots of the upper second bicuspid and upper third molar. On the right side 




Fig. 438.— Case 3. A, left; B, right. 

a number of foci of infection could be detected in the lower and upper jaws. 
All the teeth that were considered responsible for the conditions herein 
described were extracted and the improvement that followed was so marked 
that he was permitted to become a member of the household in the institu- 
tion for the aged, to which admission had been denied him some months pre- 
viously. 

Case 4 (Fig. 439) 
Woman, aged about thirty, gave a history of rheumatoid arthritis with 
marked pain in the region of the shoulder blades; pseudoankylosis ; marked 
anemia, fatigue, lassitude, etc. This case also exhibited marked reflex nervous 
manifestations. From this case Streptococcus viridans was isolated. The tooth 
that was considered beyond therapeutic measures (the lower left second molar) 



mmm 



558 



DENTAL PATHOLOGY 



! 



was extracted; some of the other teeth, the seat of chronic septic inflamma- 
tions, were treated in the approved ways, while the apices of the single 
rooted teeth were amputated. The improvement which has followed is 
most encouraging. 




Fig. 439.— Case 4. 




440.— Case 5. 



Case 5 (Fig. 440) 

Man, aged fifty years, complained of pain in the shoulder on the same 
side as that upon which was found to exist a chronic septic focus around the 
apical third of a lower bicuspid tooth. Removal of the tooth was followed 
by complete recovery. 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 



559 



Case 6 

Woman, aged about forty, gave a history of no pain, but on the other 
hand, one of disturbance of nutrition, accompanied by anemia. Being the 
wife of a physician, her case was studied with particular care by a number 
of medical practitioners, all of whom reported absence of visceral lesion. 
Several foci of infection were found in the mouth, namely, one around the 
roots of the lower first bicuspid, one around the roots of the lower right 
second molar, and one on the distal side of the upper right second bicuspid. 
Eradication of these areas was followed by decided improvement. 

Case 7 

Woman, aged thirty years. This patient exhibited symptoms of intense gen- 
eral toxemia for a number of months. Prior to the onset of these symptoms she 
reported having been in good health. She was referred to us to ascertain 
whether the condition of the lower first molar, which had been treated and 




Fig. 441.— Case 7. 



the root canals filled, was satisfactory. Suspicion had been aroused because 
the tooth was slightly tender to percussion. While a slight infection was 
present in this tooth, the main difficulty was, however, in the second bicuspid 
(Fig. 441). This patient was in such an exhausted condition as to require 
anywhere from sixteen to twenty -four hours of sleep a day, and even after 
such a long period of quietness she would awake with a feeling of fatigue as 
intense as it seemed to be at the time of retiring. The lower second bicuspid 
was extracted, and in the course of a few weeks the symptoms entirely dis- 
appeared. She has since reported that eight hours of sleep satisfy her com- 
pletely. 

Case 8 (Fig. 442) 

Man, aged about forty-five, gave a history of lameness in the right shoul- 
der, torticollis, and a continued toxic condition. He did not have to state 



560 



DENTAL PATHOLOGY 



that he was a sick man — it was self-evident. The roots of ths first molar 
showed an intensified septic process. The tooth was extracted, and there 
followed in due time a marked improvement. 




Fig. 442.— Case 8. 




Fig. 443.— Case 9. 



Case 9 (Fig. 443) 
Man, aged about forty-five years, had symptoms of toxin absorption and 
slight pain on the left side of the mandible. A large septic focus was found 
between and below the roots of the lower first molar. Extraction was fol- 
lowed by recovery. 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 561 

In a series of three hundred eases of gastrointestinal lesions, 
50% per cent, or about 152 patients, had mouths in which focal 
infections were present. Nineteen out of twenty patients suf- 
fering from ulcers were found also to be sufferers from pyorrhea. 7 

Mouth infection is probably a predisposing cause of cancer. 
In those cases a chronic infection of the alimentary tract is pro- 
duced and maintained by the infectious oral conditions, the gas- 
trointestinal infection acting as the irritant which brings about 
the proliferation of the cancer cells. 

In the prevention and treatment of tuberculosis it is of primary 
importance to eliminate, so far as possible, any additional sources 
of infection in order that the patient should not be subjected to 
the additional drain on his vitality by the subconscious effort to 
ward off infections additional to the chronic one from which he 
suffers. It is for this reason that physicians with the proper con- 
ception of the etiology, pathology, and treatment of tuberculosis, 
endeavor to not only treat the specific infection, but coincident 
therewith aim at the eradication of all other sources of chronic 
infection — of course herein including infections in and about the 
teeth. Chronic infections of the gingiva' and gums, chronic ab- 
scesses on the roots of teeth, and chronic infections in the tonsils 
and surrounding structures, must be eliminated if any degree of 
success is to be attained from the measures instituted to arrest 
the tuberculous process. II is also very probable that the lesions 
above mentioned are instrumental in the incidence of tuberculosis, 
and therefore in the battle of prevention and cure every effort 
should be made to ascertain whether chronic foci of infection are 
present anywhere in the body, and if present, no compromise 
should be reached other than their complete eradication. 
Whether the oral foci of infection are directly instrumental in 
inciting the lesion, or whether indirectly, by lowering the vital 
resistance of the individual, it matters not, to any extent, so far 
as the ultimate purpose of treatment is concerned: in either case 
all untoward conditions should be eradicated, since they are di- 
rectly and indirectly constant sources of danger to those in whose 
mouths thev are located. 



r Read, J. Marion.: Jour. California State Dental Association. 



562 DENTAL PATHOLOGY 

Secondary Focal Infections 

In the course of observations on the relationship of focal in- 
fections to systemic disease we are frequently confronted with 
a problem of difficult solution; viz., can it be established without 
more than reasonable doubt that the chronic dental lesion is di- 
rectly responsible for the onset of the systemic involvement of 
which the patient may at the time be the sufferer, and is it a 
somatic involvement ? The general practitioner has only one way 
of reaching conclusions, and that is on the basis of the clinical 
results which follow his dental interventions. If after a reasona- 
ble period of time the anticipated improvements do not material- 
ize, then ipso facto he concludes that the diagnosis of the etiology 
of the general disease was erroneous ; on the other hand, if the 
patient shows improvement, the chronic infections in and around 
the teeth must have been the sources of infection of the lesions 
in the circulatory system, gastrointestinal, respiratory, or genito- 
urinary tracts, or in articulations, muscles, nerves, or what not. 

It is of the greatest importance in the consideration of focal 
infections to bear clearly in mind (1) that the absence of im- 
provement, clinically observable, does not prove that the foci of 
infection are not etiologic factors of the disease, and (2) that the 
amelioration of the general symptoms does not prove that the foci 
under suspicion are somatically related to the systemic involvement. 
There are other factors and possibilities which must be carefully 
considered if a more correct determination is to be made of the 
relationship of focal infections to systemic disease. 

Among the many sources of infectious metastases from the 
head, the soft-tissue chronic infections in connection with the 
abnormal eruption of lower third molars is selected as an illus- 
tration, because the eradication of such a focal infection, even 
if it is the original source of a systemic involvement, is not al- 
ways followed by the disappearance or even improvement of the 
general symptoms to which it may have given rise. These so- 
called third molar abscesses bring about the involvement of the 
deep cervical lymph nodes which, in the event of becoming the 
seat of a chronic infection, establish secondary foci of infection, 
and not until this new source of absorption of bacteria and their 
toxins is removed can the general symptoms improve. There- 
fore, once a focal infection in or around the teeth, in the jaws, 



MOUTH INFECTIONS AND SYSTEMIC DISEASE 563 

air sinuses, or anywhere in the head, has been discovered, it 
is of the greatest importance to ascertain whether any secondary 
foci exist, in order that both the primary and secondary infec- 
tions may be removed at once, if at all possible or practicable. 

Another example of secondary infections in the head is to be 
found in the maxillary sinus as the result of a long standing 
periapical infection in any one of the teeth which abuts into 
it. A first molar may be the seat of a chronic dentoalveolar ab- 
scess, suspected of being the source of an existing arthritis. The 
maxillary sinus may or may not appear clear on the radiogram. 
The first molar is extracted, the floor of the maxillary sinus is 
probed to ascertain whether an opening exists through the fun- 
dus of the alveolus or not. Then, in the absence of this, the sinus 
is declared healthy, at least in so far as infection communicated 
from that first molar is concerned. As a matter of fact the 
mucoperiosteum of the sinus may be the seat of a chronic in- 
fectious process from that same molar, even in the absence of 
a macroscopic opening, and may be the seat of a focal infection 
not always detectable in a radiogram. Therefore, in the case of 
chronic abscesses upon the roots of such teeth as are in proximity 
to the maxillary sinus, the condition of the mucoperiosteum of 
the sinus should be thoroughly investigated both clinically and 
radiographically. Radiograms examined by the author, when 
showing involvement of the maxillary sinus, have in many cases 
proved to be unreliable and misleading. If the dentist is unable 
to reach a conclusion on the basis of a combination of clinical 
and radiographic examination, the services of a specialist in 
rhihology should be enlisted. 

These secondary focal infections may be located in the head in 
more or less close proximity to the dentoalveolar abscess, or in 
areas of the body at a distance from the original focus, e.g., a 
secondary focus from the original dental or oral focus in the 
gallbladder or in the appendix. 

From the foregoing we are led to the conclusion that the 
eradication of a chronic dentoalveolar abscess, or abscesses cor- 
rectly suspected of being the cause of some form of systemic in- 
volvement, will not be followed necessarily by an improvement 
of symptoms until the secondary foci to which they may have 
given rise are likewise eliminated. Because the symptoms do 



564 DENTAL PATHOLOGY 

not improve is not sufficient evidence that the dental chronic 
infections, intraosseous or extraosseous, are not primarily re- 
sponsible for the systemic derangements. 

Concerning the somatic phase of focal infections, namely, as 
to whether the infecting organisms and their toxins actually 
reach by way of an anatomic route the area in which they mul- 
tiply; or whether their pathologic significance is the result of 
additional stress placed upon the body defences, thereby de- 
creasing the chances for bacterial destruction and tissue repair 
in areas previously infected from other sources — one conclusion 
only can be reached. The dental and oral foci, whether the source 
of somatic infection, or whether they act by decreasing the effi- 
ciency in numbers of the antibodies in the blood and tissues, must 
be eliminated. The latter possibility has been conclusively 
proved under the writer's observation in his many cases of ac- 
tive tuberculosis and gastrointestinal derangements, which im- 
proved markedly, showing an arrestment of the tuberculous proc- 
ess folloAvino- the eradication of extraosseous oral foci. 



CHAPTER XLV 

DISEASES OF THE GINGIVA, GUMS, AND ORAL MUCOUS 

MEMBRANE 

Elsewhere in this work the gingivae and gums have been studied 
when in a condition of health as well as when the seat of disease 
processes which, by continuity, eventually involve the peridental 
membrane and alveolar process. In this chapter it is the aim 
in view to discuss those diseases of the oral mucous membrane 
in which large areas of tissue, relatively speaking, are eventually 
involved, giving rise to a gingivitis, a stomatitis or to a combina- 
tion of both processes. Gingivitis, we define, therefore, as an in- 
flammation, acute or chronic, of the gingivae or gums or both 
structures; and stomatitis, as an inflammation, acute or chronic, 
of the mucous membrane which lines the floor of the mouth, 
cheeks or palate. Most forms of stomatitis develop in the period 
from infancy to childhood, although in adults some of the most 
severe forms, accompanied by ulceration and sloughing of tissue 
are encountered. The mucous membrane of the cheeks, lips 
and the alveolar process may be involved in their entirety in 
certain forms of the disease ; in others only limited areas are 
affected. The varieties of stomatitis generally encountered are 
the simple, catarrhal, aphthous, mycotic, ulcerative, mercurial, 
and gangrenous. 

Simple Stomatitis (Stomatitis Simplex) 

A hyperemia condition of the oral mucous membrane, which if 
not corrected when it first appears, acquires the characteristics 
of the catarrhal form. The membrane is sensitive, especially to 
hot and acid or pungent foods. It may develop in the course of 
the eruption of the deciduous or permanent teeth, it being asso- 
ciated with the gastric and intestinal disturbances which are in 
some cases the accompaniments of so-called pathologic dentition. 
Fever may be present when it develops in children, and either 
diarrhea or constipation accompanies it. In adults the ingestion 
of highly spiced foods and intemperance in the use of tobacco 

565 



nn 



566 DENTAL PATHOLOGY 

and alcohol are some of the etiologic factors of this form of 
stomatitis. The disease may last from a few hours to a few days, 
but subsides shortly after the elimination of the cause. 

Pathologic Anatomy. — The characteristic feature of the disease 
is the dilatation of the blood vessels of the connective-tissue mat 
of the mucous membrane, the result of the presence in the mouth 
of some form of irritation, which, if not eliminated, decreases the 
vital resistance of the tissues and prepares the field for subse- 
quent bacterial infection. Areas of elevated mucous membrane 
may be distributed throughout the mouth. It should be borne 
in mind that a simple stomatitis is the antecedent of the catar- 
rhal (infectious) form, and that from its etiology bacterial irrita- 
tion is excluded. Therefore, in addition to the etiologic factors 
already mentioned, must be added the irritation caused by de- 
fective partial or full plates, concentrated germicidal solutions 
used as mouth washes, and salivary deposits impinging upon the 
gum tissues. While not in line with the aims of this book to 
enter into therapeutic discussions, it may nevertheless be ad- 
visable to suggest a general line of treatment which in the case 
of simple stomatitis should be undertaken as soon as the first 
symptoms of the disease appear. All sources of irritation, me- 
chanical or chemical, should be at once eliminated, and the teeth 
should be subjected to a thorough scaling and polishing. An 
antiseptic mouth wash should be prescribed, either a light purple 
potassium permanganate solution (1:3500), or a potassium chlo- 
rate solution 2:100. 

Catarrhal Stomatitis 

Any one of the etiologic factors mentioned in connection with 
the simple form of stomatitis, when permitted to persist, or a com- 
bination of two or more of these etiologic factors plus bacterial 
infection, are responsible for the onset of catarrhal stomatitis. 

There is, besides redness of the mucous membrane of the palate, 
floor of the mouth, cheeks and gums, all of the symptoms and 
manifestations of a well-established infectious inflammation. 
There will be swelling, rise in temperature from one to four de- 
grees, pain upon mastication, increased flow of saliva, spongy 
texture of the gums, increased sensitiveness of the mucous mem- 
branes at all times, even to the point of making mastication im- 



567 

possible, fetidity of the breath; in some cases instead of an 
increased flow of saliva, the month will feel dry and hot and an 
abundance of thick and stringy mncus will be present, This 
form is generally associated with disturbances of digestion and 
whether it occurs in children or adults, neglect of the teeth and 
investing tissues is the paramount etiologic factor. Chronic dis- 
orders such as tuberculosis, syphilis, diabetes may act as predis- 
posing causes by reason of the lessened resistance of individuals 
so affected. 

Pathologic Anatomy. — A marked congestion of the mucous 
membrane and an excessive mucus discharge are the salient 
phenomena in this form of stomatitis. Epithelial desquamation 
and edema are present. Mucoid degeneration of the superficial 
epithelium and of the alveolo-tubular glands occurs. If many 
polymorphonuclear leucocytes in various stages of degeneration 
are present, the discharge assumes a whitish or yelloAvish color. 
Following the elimination of the cause or group of causes, a re- 
generation of the lost superficial epithelium occurs and the mu- 
cous membrane again resumes its normal color and texture. 
Catarrhal stomatitis is frequently an accompaniment of scarlet 
fever, measles, smallpox, and typhoid fever. 

Ulcerative Stomatitis (Fig. 444) 

Ulcerative stomatitis is an intense inflammation of the mucous 
membrane, accompanied by ulceration and destruction of soft 
tissue by gangrenous decomposition. 

In ulcerative stomatitis the systemic factor plays an important 
part. It does not occur unless the vitality is greatly reduced by 
some general disease. It may follow the continued administra- 
tion of mercury, especially if the teeth and the mouth, as a whole, 
were not placed in good condition before the treatment was be- 
gun. The neglect of the hygiene of the mouth through insuffi- 
cient brushing, the presence of salivary and subgingival deposits, 
excessive smoking and drinking, or in children's diseases of 
nutrition, the exanthemata, etc., are factors of importance in the 
etiology of the disease. 

The ulcers in ulcerative stomatitis start upon the gingival tis- 
sues as a rule, although they may be located upon any part of 
the mouth, the buccal or palatal mucous membranes, the floor of 



568 DENTAL PATHOLOGY 

the mouth and upon the tongue. The affected gingival margin 
shows a dark yellow or greenish appearance. Ulcerative stoma- 
titis is contagious and frequently spreads to members of a 
family, and it assumes^epidemic form among soldiers, in factories, 
and wherever large bodies of men congregate. 

The disease is not strictly local. General symptoms character- 
istic of toxemia are frequently present. There may be intestinal 
symptoms, viz., lack of appetite, rise in temperature, and profound 
depression. The gangrenous decomposition of the ulcerated areas 
gives off a very offensive odor and the tissues of the mouth be- 
come so painful as to render impossible the mastication of food. 
The infection may spread to the periosteum, causing destruction 
of the alveolar process and the loosening of the teeth, especially 
in young children. 

It develops occasionally in the course of pyorrhea alveolaris 
following an exacerbation of the otherwise chronic infection 
characteristic of that disease. Among the chief etiologic factors, 
must be mentioned neglecting the teeth, the presence of cavities, 
and sharp edges of fillings, crown, etc. 

A suggestion as to treatment may not be out of place. It 
should consist of local and systemic measures. The local measures 
should include the following steps: 

1. Thorough sealing and polishing of the teeth. 

2. Temporary fillings Avhere needed. 

3. 10 to 20 per cent silver nitrate applied to the ulcerated tis- 
sues, or a 10 per cent glveerinated salvarsan, or liquor potassii 
arsenitis. 

4. Frequent irrigations of the mouHi with potassium perman- 
ganate solutions of proper strength (1:3500). 

The systemic treatment should include : 

1. Rest, nonirritating diet, abstinence from tobacco and alcohol. 

2. Laxatives to insure complete elimination. 

3. Administration internally of potassium chlorate, 1 teaspoon- 
full every three hours, of a solution of 24 grains to the ounce. 
For children reduce the dose to 12 grains to the ounce. 

Pathologic Anatomy. — The anatomic lesion in ulcerative stoma- 
titis results from the infection of any portion of the gingival 
mucous membrane by several organisms, especially staphylococci, 
streptococci, the Bacillus fusiform is and the spirilla of Vincent. 




Fig. 444 — Ulcerative stomatitis. (After Preiswerk.) 



GINGIVAE, GUMS AND ORAL MUCOUS MEMBRANE 569 

The gingival margins are the usual locations for the beginning 
of the infection and may involve the gingivae over only a few 
teeth, or in extreme cases, the entire gingivae may be affected. 
The tissues show evidences of gangrenous decomposition which 
follows the destruction of life in the tissues by bacterial activity. 
In rare cases the gums remain unaffected, the buccal and palatal 
mucous membrane being then the tissues involved. The gingivae, 
when it is the seat of the infection, appears covered with a yel- 
lowish fibropurulent exudate. The inflammatory process is not 
limited to the area immediately adjacent to the tissues undergo- 
ing gangrene, but the entire mucous membrane may appear 
deeply inflamed. High temperature, loss of appetite, mental de- 
pression, and extreme fetidity of the breath, are the accompany- 
ing symptoms. 

Mercurial Stomatitis 

Mercurial ptyalism — mercurial salivation — is an infection of the 
mucous membrane of the mouth, following decrease in resistance 
against infection brought about by the irritating effects of mer- 
cury and its compounds when administered for a prolonged period 
in the treatment of syphilis. The salts of mercury are eliminated 
in part by the saliva, and when their use has been constant for 
months, the mucous membrane is constantly and continuously 
subjected to the irritating action of these compounds. The first 
symptoms of mercurial ptyalism consist in redness of the mucous 
membrane, offensive breath, a generalized pericementitis over all 
the teeth, and an increase in the flow of saliva. If the administra- 
tion of mercury is not discontinued, the gums ulcerate, and the 
peridental membranes become so weak and relaxed that the teeth 
appear to be ready to drop out. The infection spreads from the 
peridental membrane to the alveolar process, and in severe cases 
exfoliation of sequestra takes place. The tongue may be swollen 
and the seat of ulcerations, and the salivary glands, especially the 
parotid, may become swollen and inflamed. The symptoms of 
ptyalism set in relatively early during the administration of mer- 
cury if the mouth has been neglected, i.e., in the presence of cavities, 
infections of the peridental membrane, salivary and subgingival 
deposits, broken-down crowns and teeth. It also develops among 
workmen in the industries in which mercury is employed. The 
infection is polymicrobic in character. 



570 DENTAL PATHOLOGY 

Aphthae — Canker Sores — and Aphthous Stomatitis 

Individual aphthae, or canker sores, are localized disturbances 
of the oral mucous membrane, the manifestations of some form 
of mild irritation. An aphtha is a small rounded vesicle, white 
or gray in color, which begins as a hyperemic spot and subse- 
quently, because of degeneration of the superficial epithelium, with 
a fibrinous exudate, assumes the appearance of a white or grayish 
vesicle. The vesicle in a few days collapses or breaks down, ex- 
posing an ulcerated under structure. At the beginning of the 
eruption the hyperemic spots are sensitive to sour or sweet food- 
stuffs, the patient's attention being first called to their existence 
by their sensitiveness. One or a number of aphtha? may develop 
in one or several areas of the mucous membrane, such as on 
each side of the frenum of the tongue, on the margin of the 
tongue, on the internal surface of the lips, especially on the 
lower; rarely on the internal surface of the upper lip or upon 
the gums. The sjmrptoms to which the aphthae give rise are very 
light, and in a few days the disorder disappears. 

Aphthous stomatitis, or an inflammation of the oral mucous 
membrane, accompanied by the formation of vesicles or aphthae 
which may join or coalesce, each surrounded by a reddish mucous 
membrane, develops in poorly nourished infants and children in 
connection with the eruption of the teeth, or following such ex- 
haustive diseases as whooping cough or bronchopneumonia. In 
adults it may develop in pregnant women. 

Pathologic Anatomy. — It is not uncommon to find in the litera- 
ture that aphthous stomatitis and thrush are described as iden- 
tical diseases and of identical pathogenicity. This is indeed a 
mistake, as the disease under consideration is not the manifesta- 
tion of a mycotic infection, but a probable superficial infection 
by any one of a number, or combinations, of mouth organisms. 
Hyperemic spots here and there, areas of congestion, stagnation 
and consequent decreased tissue resistance and subsequent in- 
fection, fibrinous effusions, degenerated and dead epithelium in 
the vesicular formations — summarize the pathologic features of the 
disease. 



GINGIVAE, GUMS AND ORAL MUCOUS MEMBRANE 571 

Thrush 

Thrush is an infection of the mucous membrane of the mouth 
caused by the saccharomyces albicans (oiclium albicans) which de- 
velops in athreptic infants and weakened adults. It is charac- 
terized at the beginning by extreme dryness of the mouth (partial 
arrestment of salivary secretion) and an annoying sensation of 
intense heat. The tissues of the mouth become red and the tongue 
papilla? project above the surface. The patches themselves may be 
small, or they may coalesce, covering the area in which they are 
located with a whitish deposit. On account of the abundance of 
a white discharge of a fibrinous nature, or wherever the sac- 
charomyces is active and multiplying, the name of creamy stoma- 
titis has been given to this form of stomatitis by French writers. 
It is by this name that stomatitc crcmcusc is described in the older 
and in some of the recent French textbooks. The patches may 
develop on aiw portion of the tongue, lips, cheeks, floor of the 
mouth, palate, hard or soft, perhaps on the gums and even in the 
throat or pharynx. The patches, at first white, later assume a dark 
color. Frey 1 has observed many cases of the disease, and from 
the original in French we quote as follows: "The systemic in- 
volvement varies according to the patient's age. In the new- 
born there may be difficulty in nursing and deglutition, diarrhea, 
vomiting; in the adult the sensation of dryness is very marked. 
In the aged, especially those affected with chronic disorders of 
the urinary tract intense dysphagia is present, especially in con- 
nection with the ingestion of food requiring mastication and iii- 
salivation. Two forms are observable in children, one in well 
nourished infants simultaneous with the presence of colic, diar- 
rhea and vomiting of short duration and another form in poorly 
nourished infants suffering from persistent diarrhea, vomiting, 
abdominal tympanitis and all other manifestations of serious di- 
gestive disturbances. ' ' 

The acid fermentation of milk and starches in the mouth is 
closely associated with the development of thrush, as the sac- 
charomyces albicans finds in that kind of medium a soil favorable 
for its growth and development. It should be remembered, how- 
ever, that while decided alkalinity arrests the growth of the sac- 



1 Pathologie de la Bouche et des Dents. 



572 DENTAL PATHOLOGY 

charomyces, it may continue to grow in a mildly alkaline or 
neutral medium. 

Pathologic Anatomy. — The stratified squamous epithelium of 
the mucous membrane becomes the seat of a fibrinous inflamma- 
tion, brought about by the growth and development within it- 
self of the saccharomyces (oidium) albicans. Degeneration and 
loss of superficial epithelium occurs, and the infection may spread 
into the underlying connective tissue. The membranous charac- 
ter of the patches is the result of the fibrinous type of inflamma- 
tion to which the organism gives rise. 

Herpes Labialis 

Herpes labialis (lip herpes) is a circulatory disturbance over 
limited areas of the lips caused by deranged nervous function. 
They have the appearance of blisters. The epithelium is raised 
and if scraped off or when it sloughs off, it exposes an irritated 
connective-tissue understructure painful to the touch and bleed- 
ing readily. These are also known as cold sores, fever sores or 
fever blisters. The decreased or arrested secretion of the epi- 
thelial glands of the mucous membrane of the lips deprives the 
lips of necessary lubrication and protection against air and dust 
particles with a consequent irritation to the nerve endings, re- 
sulting in the canker sore or fever blister. These sores occur upon 
the lip during or following colds, fevers, typhoid, or the use of 
the rubber-dam for prolonged sittings. The tissues of the lips 
become abnormally dry and crack open on the slightest provoca- 
tion. 

Affections of the Tongue 

The tongue may be the seat of deformities which interfere with 
speech. This is due to a short frenum which prevents the tongue 
from being protruded in the act of speaking. The tongue may 
have a deep median fissure — a cleft. The complete absence of 
the tongue has also been reported. 

Ulcers of the Tongue 

Simple ulcers of the tongue are usually the result of irritation 
by a jagged tooth, crown, or some foreign body in the mouth. 
They persist until the irritant is removed. Following the de- 



GINGIVAE, GUMS AND ORAL MUCOUS MEMBRANE 573 

struction of the superficial epithelium they become infected, and 
in people past the age of thirty or thirty-five they should be 
considered dangerous, as they are liable to mark the beginning 
of the development of malignant neoplasms. In making the diag- 
nosis of these ulcers an accurate history of their development 
should be secured, and if upon removing all sources of irritation 
and treating them with weak silver nitrate solutions they do not 
disappear promptly, the prognosis is serious. If there be no in- 
duration the ulcer is probably a benign one, but if induration be 
present it is probably a malignant one. Ulcers of the tongue may 
also be syphilitic, in which case the history, the presence of other 
manifestation of syphilis, and the Wassermann test, will determine 
the diagnosis. Indurated ulcers in patients past forty years of age 
suspected of being carcinomatous, should be excised without de- 
lay. 

The tongue is frequently the seat of inflammatory disturbances 
brought about by digestive disorders. In these cases the tongue 
appears red and smooth, the inflammation being as a rule located 
in the anterior portion of the tongue. 

Leucoplakia of the Tongue 

Leucoplakia is a disease characterized by the presence upon 
the dorsum of the tongue and mucous membrane of the mouth, 
particularly the buccal, of patches of a yellowish Avhite color, 
irregular in shape, and slightly raised above the mucous mem- 
brane. They may become indurated, and after the white patches 
are cast off, the under-surface so exposed appears ulcerated. 
The superficial layers of the stratified squamous epithelium arc 
thickened, while the dee]) layers exhibit a tendency to proliferate 
into the deeper structures. The patch may also have a bluish 
color and whenever it is removed, whether it be the white patch 
or the bluish, it leaves a raw surface behind. There is no pain 
accompanying the patches. It may be caused by the irritation 
of tobacco smoke, strong drinks or highly spiced food, or it may 
be a manifestation of a long standing syphilis. Some authorities 
consider leucoplakia as a forerunner of cancer — a precancerous 
lesion — and consequently insist upon the complete excision of the 
patches, while others believe that leucoplakia is the oral manifes- 
tation of psoriasis. 



INDEX 



Abnormalities of teeth, 250 

of upper lateral incisor, 267 
Abraded surfaces, shape of, 357 
Abrasion and malocclusion, 356 
Abrasion and pulp exposure, 357 
cup-shaped in lower molars, 362 
etiology of, 356 
from chewing gum, 356 
from gritty tooth-powders, 356 
from pipe and cigarette stems, 356 
from tooth-brush friction, 356 
in cuspids, 360 
in incisors, 358 
of root, 357 

pathologic anatomy of, 357 
pulp degeneration in, 358 
tubular calcification in, 358 
Abscess, acute dentoalveolar, 424 

and chronic, difference in pathol- 
ogy, 443 
bone involvement in, 457 
clinical symptoms of, 425 
definition of, 424 
discharge from, 424 
discharging externally, 429 
discharging into maxillary sinus. 

427 
discharging into nasal cavity, 

427 
extensive swelling from, 431 
involvement of face in, 429 
limited swelling from, 431 
most painful stage of, 431 
protrusion of tooth in, 433 
periostitis in, 435 
chronic dentoalveolar, characteris- 
tics of, 443 
cultures from, 454 
etiology of, 436 
fibrous wall of, 451 
forms it may assume, 438 
looseness of tooth with, 440 
leucocytes in mass of, 444 
microscopic anatomy of, 444 
pathologic anatomy of, 436 
sequestrum formation in, 468 
sinus formation in, 427 
staphylococci in, 4.12 
streptococci in, 4-">2 
sinuses from, 436 



Abscess — Cont 'd. 

formation, 102 

"hot," 103 

lateral, 422 

periapical chronic, 423 

pericemental, 422 

pyorrheal, 422 

sinusless, chronic dentoalveolar, 549 

subacute dentoalveolor, 430 

chronic dentoalveolar, systemic in- 
volvement by bacteria from, 
551 
Abscesses, blind, 549 

chronic, trabeculated, 451 

cold, 103 
Absence of teeth, 291 
Acari, 196 
Acarus, scabiei, 206 
Acid, dilute, action upon enamel, 219 

effects of, on enamel, and permea- 
bility of, 227 

lactic in erosion, 360 
Acidity, potential, of salivary depres- 
sants, 312 

producers, .".L'4 

weak, in mouth washes, 332 
Acroo dextrin, '.'<'2'2 
Actinomyces bovis, 181 
Actinomyces Madura, 182 
Actinomycosis, 181 
Adamantinoma, 146, 535 
Adenoearernomata, 143 
Adenoma, acimise, 139 

alveolar, 139 

canalicular, 139 

racemose, 139 

simple, 139 

tubular, 139 
Adenomata, 138 
Adhesions, 107 
Age and dental caries, 320 
Age as a predisposing cause of dis- 
ease, 38 
Agenesia, 46 

of enamel, 256 
Agglutinins, 153 
Albumen in normal and pathologic 

saliva, 371 
Albuminoids, 28 
Alkaloids, animal, 524 

cadaveric, 413 



575 



576 



INDEX 



Albuminosis, 64 

Albumins, 28 

Alveolar plate, exfoliation of, 462 

process, atrophy of, 491 
Alveoli, cortical layer of, 461 

necrosis of, 462 
rarefying osteitis of, 462 
Alveolodental periosteum, 402 
Ameboid movement, 32 
Ameloblasts, 245 
Amino-acids, 27 
Ammonium carbonate in hyperacid 

diathesis, 372 
Amyloid degeneration, 56 
Anasarca, 95 
Anatomy, pathologic, 37 

definition of, 213 
Anemia, collateral, 82 

local, 82 

neurotic, 82 

idiopathic, 82 

obstructive, 82 
Angina, Vincent 's, 179 
Angioma, cavernous, 134 
Angiomata, 133 
Angiosarcoma, 126 
Ankylostomiasis, 203 
Anopheles, 188 
Anthrax, 176 
Anthracosis, 64 
Antibodies, 153 
Antigens, 153 

Antiseptic power of saliva, .'515 
Aphthae, 570 
Aphthous stomatitis, 570 
Apical areas, resorption of, 465 

region, pyogenic bacteria in, 412 
Aplasia, 46 
Arachnida, J 96 
Argvria, 64 
Arterioliths, 381 
Arthritis deformans, 554 
Arthritis from oral foci of infection, 

563 
Arthritis, infectious, cas3 histories, 

554 
Arthropoda, 196 
Ascaris lumbricoides, 200, 201 
Ascites, 96 

chylous, 95 
Ateleiosis, 45 

Atmospheric pressure, increased, ef- 
fects of, 43 
Atrophy, 41 

brown, 46 

combined, 45 

degenerative, 45 

discussion of, 250 

etiology of, 46 



Atrophy — Cont 'd. 

general, 45 

gross morbid anatomy of, 46 

local, 45 

numerical, 45 

pathologic histology of, 46 

pathologic physiology of, 47 

simple, 45 
Autolysis, 76 

B 

Bacillus acidophilus, 324 

anthracis, 176 

coma, 176 

diphtheria, 173 

dysenteric, 175 

fusif ormis, 179, 452 

gangrenae pulpae, 452 

gingivae pyogenes, 452 

influenza, 178 

pestis, 177 

of Ducrey, 158 

pulpae pyogenes, 452 

pyocyaneus, 155 

tuberculosis, 164 

typhosus, 174 
Backward caries, 328 
Bacteria, 152 

from chronic dentoalveolar abscess, 
551 

higher, 153 

in dentinal tubules, 328 

lower, 153 

on the number of, in mouth, 315 

putrefactive, 79 

pyogenic in apical region, 412 
Bacterial absorption from subgingival 
space, 380 

enzymes in dentin caries, 326 

infection, nonreceptivity to, 214 
Bacteriemia, 154 
Bands of Eetzius, 221 
Betel-nut chewing, 383 
Bicuspid, abrasion of, 362 

lower first, abnormalities of, 277 

lower first, hypoplasia of, 277 

lower second, hypoplasia of, 277 
Bicuspids, lowci', with two roots, 277 

perfect fissures in, 318 

second, impaction of, 297 

upper first, with three cusps and 
roots, 271 

upper, hypcrcementosis in, 351 

upper, hypoplasia of, 274 

upper second, abnormalities of, 271 
bifurcation of root of, 273 
with two or three roots, 274 

upper, with three roots, 273 



INDEX 



577 



Biliary, calculi, 70 

Blastodermic layers, 34 

Blastomyeetes, 152 

Blastomycosis, 152, 182 

Blind abscess, 436 ~ 

Blood cells, solution of, by saliva, 315 

coagulation, 74 

excess of carbon dioxide in, 362, 363 

hemolytic power of, 315 

suffusion of, 86 

supply of peridental membrane, 402 

uric acid salts in, 496 
Bone and cementum, differences be- 
tween, 233 

cancellated, 455 

changes in maxillary sinus, 427 

compact, 455 

corpuscles of, 4-55 

endochondral, 456 

lamella? of, 4.15 

lesions in pocket formation, 394 

normal and pathologic considera- 
tions, 4.15 

periosteal, 456 

spongy, 455 
Bright's disease, 95 
Bioblasts, 25 
Broncholiths, 70 
Bronchopneumonia, 161 
Bubonic plague, 177 
Burns, degrees of, 42 



Cadaverin, 413, 524 
Caisson disease, 4.'! 
Calcareous deposits, 381 
in intestines, 381 
formations in pulp hypertrophy, 531 
infiltration, 68 
Calcicosis, 64 
Calcification of enamel, direction of. 

246 
Calcification, tubular, in abrasion, 358 
Calcified amorphous bodies in defec- 
tive iissuivs. 260 
Calcium acid phosphate in erosion, 

361 
Calculi, biliary, 70 
renal, 70 
vesical, 70 
Canaliculi in cementum, 234 
Canals, Volkmann's, 4.1.1 
Cancellated spaces, infection through. 

418 
Cancer and mouth infection, 561 
Cancer, colloid, 140 
Candv-makors mouth, 312 



Canities, 67 
Canker sores, 570 

Carbohydrate diet, excessive, manifes- 
tation in saliva, 374 
Carbohydrates, degrees of fermenta- 
tion of, 323 
Carbon dioxide, excess of, in blood, 

362 
Carbuncle, 103 
Carcinomata, 139 

basal cell, 142 

medullary, 145 

scirrhous, 143 

simple, 146 
Caries, among civilized races, 311 

among school boys and girls, 313 

ancient theories of, 307 

and age, 320 

and diet, 311 

and general diseases, 321 

and heredity, 321 

and inflammation of gingivae and 
gums, 320 

and osteomalacia of pregnancy, 320 

and starchy foods, 320 

and sulphocyanates, 371 

and the constitutional factor, 314 

backward, 328 

beginning of, 334 

chemico-bacterial theory of, 314 

ehemico-parasitie theory of, 310 

coarse foods in relation to, 312 

conditions which favor progress of, 
317 

.(institutional factor in. 414 

dissolution of enamel in, ."'>22 

etiologic factors in. 322 

factors which favor. .'114 

favorable areas for. :!14 

historical data, 306 

how it advances, 357 

how limited, 355 

immunity from, 315 

immunity to, in uncivilized races, 
311 

in approximal surfaces, predispos- 
ing causes of, 336 

in British races, 313 

in candy-makers and millers, 312 

in dentin, progress of, T142 

in fissures and pits, 334 

in meat-eating tribes, 312 

in prehistoric times, 311 

in teeth of uncivilized races, 224 

in the Maori race, 313 

lateral, 326, 328 

malocclusion and, 319 

Miller's conclusions on, 310 



578 



INDEX 



Caries — Cont 'd. 

of dentin, 340 

of dentin, bacterial enzymes in, 326 

onset of conditions which favor, 320 

pathologic processes in, 322 

predisposition to, of hypoplastic 
enamel, 318 

predisposing causes of, 317, 320 

pulp infection in absence of, 527 

putrefaction theory of, 309 

quantity of saliva in relation to, 
316 

races free from, 312 

restricted, 320 

role of ptyalin in, 370 

salivary stimulants in relation to, 
312 

statistics on, 313 

teeth in malocclusion and, 319 

theories on, accepted, 310 

worm theory of, 309 
Carious process in dentin, 326 
Cessation, 76 
Catarrhal stomatitis, 566 
Causes of disease, 37 
exciting, 37, 214 

of hypercementosis, 353 

of pericemental inflammation, sep- 
tic, summary of causes, 421 

predisposing, 37, 213 

predisposing, of caries, 317 

predisposing, of caries in approxi- 
mal surfaces, 323 

predisposing, of dental caries, 320 

predisposing, of dental disease, 215 
Cell, 23 

anatomy of, 24 

chemistry of, 26 

growth, 32 

nutrition of, 32 

physics of, 29 

physiology of, 32 

staining reactions of, 30 

wall, 24 
Cells, cementoclastic, 250 

giant, 456 

plasma, 451 
Cementoblasts, 233, 407 
Cementoclastic cells, 250 
('omentum, 233, 248 

and enamel, line of junction, 228 

canaliculi of, 234 

caries of, 349 

changes, conditions which govern, 
250 

chemical composition of, 240 

denudation of, 388 

differences from bone, 233 



Cementum — Cont 'd. 

fibers encased in, 234 

formation of, 350 

ground sections of, 238, 239, 240 

how deposited, 233 

increases in thickness of, 250 

lacunae, 233 

lamellae, 233 

increase in number of, 355 
increase in size of, 355 

matrix of, 234 

nutrition of, 233 

nutrition to, from dentin, 237 

resorptions in, 250 
Centrosome, 25 

Cervicolingual ridge, abnormalities of, 
264 

fissured, 265 

hypoplasia of, 265 
Cestodes, 195, 198 
Chalicosis, 64 
Chancre, soft, 158 
Chancroid, 158 
Chemisis, 96 

" Chicken-fat" clots, 75 
Chicken pox, 191 
Chilblain, 42 

Chlorides, increase of, in gouty diath- 
esis, 372 
Cholera, Asiatic, 173 
Cholesteatoma, 149 
Cholestcrin, 29 
Chorionepithelioma, 149 
Chloroma, 128 
Chondromata, 120 
Chordomata, 121 
Chromatin, 26 
Chronic gingivitis, 392 
Cilia, 32 

Ciliary movement, 32 
Congenital disease, 40 
Circulatorv activity, impairment of, 
215 

changes, 82 
Cleft palate, 211 
Cloudy swelling, 48 
Coagulation, blood, 74 
Coagulation necrosis, 73 
Coceidiosis, 190 
Calco-globulin, 382 
Cold, effects of, 42 
Colloid degeneration, 52 
Colloids, 29, 30 
Coma bacillus, 173 
Concretions, 69 
Concussion, 41 
Congestion, hypostatic, 85 
Conjunctivitis, epidemic, 179 



INDEX 



579 



Constructive changes in cenientum, 250 
Contact, lack of, 379 
Cough, -whooping, 179 
Culex, (mosquito), 188 
Cusp, lingua], of lower first bicuspid, 
277 
supernumerary in upper first molar, 
280 
Cuspid, lower, supernumerary root in. 
273 
hypoplasia of, 270 
short rooted, 270 
two rooted, 270, 272 
radiograph of, 273 
Cuspids, abraded, 360 

upper, abnormalities of, 269 
longitudinal section of, 228 
short rooted, 270 
Cusps, three, in upper first bicuspid, 

271 
Crystalloids, 29, 30 
"Currant jelly" clots, 75 
Cylindromata, 147 
Cytoplasm, 23, 25 
Cystic odontomas, 532 
Cysts, 149 
dental, 532 
dental or root, pathologic anatomv 

of, 539 
dentigerous, 410, 441 
dermoid, 148 
follicular, 534 
follicular, pathologic anatomv of, 

540 
glandular, 150 
parasitic, 150 
retention, 149 
root, 532 

softening or necrotic, 150 
Czermack, interglobular spaces of, 23] 

D 

Death, somatic, 73 

Decalcification, tardy, of deciduous 

teeth, 302 
Deciduous enamel, when it begins to 
form, 246 
teeth, calcification of, 248 
retention, 291 

tardy decalcification of, 302 
Deformities, macroscopic, of central 
incisors, 264 
of teeth, macroscopic, 264 
Degenerations, 47 
amyloid, 56 
colloid, 52 
fatty, 48 



Degenerations — Cont 'd. 
granular, 48 
hyaline, 54 
mucoid, 50 
parenchymatous, 48 
waxy, bacony, or lardaceous, 56 
Dengue, 193 
Dental band, 241 

Dental caries among civilized races, 
311 
among school boys and girls, 313 
and age, 320 
and civilization, 311 
and general diseases, 321 
and heredity, 321 
and inflammation of gingiva and 

gums, 320 
and meat diet, 320 
and pregnancy, 320 
and starchy foods, 320 
and teeth in malocclusion, 319 
chemieo-bacterial theory of, 314 
coarse foods in relation to, 312 
conditions which favor onset of, 320 
conditions which favor progress of, 

317 
constitutional factor in, 414 
"dry mouth" in relation to, 316 
etiologic factors in, 322 
factors which favor, 314 
historical data, 306 
immunizing properties of saliva in, 

315 
immunity to in uncivilized races, 

311 
in British races, 313 
in candy-makers and millers, 312 
in Maori race, 313 
in meat-eating tribes, 312 
in prehistoric times, 311 
on immunity from, 315 
pathologic processes in, -".22 
predisposing causes of, 317, 320 
quantity of saliva in relation to, 

316 
races free from, 312 
restricted, 320 
salivary stimulants in relation to, 

312 
statistics on, 313 
Dental cysts, 532 
ectopia, 304 
disease, definition of, 213 

predisposing causes of, 215 
follicle, chronology of, 245, 254 
follicles in syphilitic, 305 
granuloma, 355, 436, 549 
groove, 241 



580 



INDEX 



Dental— Cont 'd. 

hypoplasia and caries, 252 
hypoplasia, definition of, 251 

microscopic, 252 
infantilism, 304 
lamina, 241 
papillae, 246 
ridge, 241 

stigmata of syphilis, 303 
Dentrifices, cause of dentin discolora- 
tion, 347 
Dentigerous cysts, 410, 441 
Dentin, 228 
caries, 340 

carious process in, 326 
caries, progress of, 342 
chemical composition of, 233 
comparative hardness of, 226 
discoloration by dentrifices, 347 
elastin in, 230 
forming organ, 246 
hypoplasia, 256 
intertubular substance of, 248 
lactic acid in depth of, 328 
matrix, 230 

matrix liquefaction of, 342 
microorganisms in the structure of, 

327 
nature of tissue, 228 
nutrition to, from cementum, 237 
pigmentation in caries, 347 
secondary, 511 

amorphous, 511 

amorphous classification of, 511 

typical, 511 
temporal- y arrest of calcification in, 

253 
the softening of, 341 
transverse section of, 229 
Dentinal fibrilhe, 228 
tubuli, 228 

a field of, 229 

anastomosis of, 230 

average diameter of, 250 

bacteria in, 238 

calcifications in, 250 

Calcific degenerations of, 510 

curves of, 231 

in bicuspids and molars, 230 

in crown portion, 230 

in incisal region, 230 

in relation to cusps, 231 

in root portion, 230 

penetration into enamel, 232 

penetration into cementum, 237 

putrefactive changes in, 414 

relative diameters of, 230 



Dentinification, process of, 247 
Dentition, complete absence of, 292 

deformities of, due to syphilis, 302 
Dentoalveolar abscess, acute apical, 
424 
acute osteomyelitis in, 435 
chronic, 436 

chronic, bacteria from, 551 
chronic forms of, 438 
chronic, systemic involvement 

from, 551 
clinical symptoms of, 425 
pathologic anatomy of, 433 
Deposit, calcareous, 381 

subgingival, lesions produced by, 
392 
Development of teeth, 241 
Diagnosis by percussion, 440 
Diapedesis, 99 
Diaphanous halo, 345 
Diathesis, goutv, increase of chlorides 
in, 372 
hyperacid, ammonium carbonate in, 
372 
Diet and caries, 311 
Diphtheria, 173 

Diplococcus intraeellularis meningiti- 
dis, 156 
Disaccharides, 324 

Discoloration from pulp putrefaction, 
524 
of enamel, congenital, 259 
of teeth, 441 

on approximal surfaces of bicus- 
pids and molars, 334 
with nonexposed pulp, 530 
Disease, cause of, 37 
congenital, 40 
contagious, 152 
definition of, 21 
dental, definition of, 213, 216 
predisposing causes of, 215 
etiology of, 37 
functional, 21, 216 
infectious, pathology of, 152 
general, definition of, 216 
of the gingivae, gums and mucous 

membrane, 565 
organic, 216 
Discuses of peridental membrane, 402 
of sal (oxidation, 361 
suppurative, 154 
susceptibility to, 214 
toxemic, 172 
Dropsy, 95 

Ducts of salivary glands, deposits in, 
381 



INDEX 



581 



Drugs, irritating, in root canal work. 

408 
Dysentery, amebic, 185 
baeillary, 175 

E 

Ear, involvement from impacted third 

molars, 297 
Eechymosis, 86 
Ectoderm, 35 

tissues derived from, 35 
Edema, 84, 95 

angioneurotic, 96 

cachectic, 96 

cardiac, 96 

ex vacuo, 96 

gaseous, 177 

lymphatic, 96 

malignant, 177 

mechanical, 96 

pulmonary, 96 

renal, 96 

toxic, 96 
Elastin in dentin, 230 
Electricity, effects of, 43 
Electrolytes, 30 
Elephantiasis, 95, 206 
Emboli, composition of, 91 

infectious, 463 

traumatic, 91 

types of, 90 
Embolism, 90 

results of, 92 
Embolus, capillary, 90 

cardiac, 90 

lymphatic, 91 

paradoxical, 91 

venous, 91 
Enamel, action upon, of dilute acids, 
219 

agenesia, 256 

and cementum, line of junction, 22^ 

brown spots in, 319 

calcification, effects of exanthemata 
upon, 253 

calcification installments, 221 

caries, etiology of, 331 
first symptom of, 332 
localization of, 334 
photomicrograph of, 333 

cementing substance in, 219 

chalky, 258 

character of external surface of, 
225 

chemical composition of, 223 

comparative hardness of, 226 

complete or partial absence of, 255 

components of, 219 



Enamel— Cont 'd. 

deciduous, when it begins to form, 

246 
defects in, from insufficiency of 

structure, 319 
deviations in quantity and quality 
of interprismatic substance, 
253 
direction of calcification of, 246 
dissolution of, in caries, 322 
fissures in, 225 
granular defect of, 263 
hypoplasia of, producing external 

defect, 255 
hypoplastic, and caries, 317 
in abnormal locations, 286 
imbrication lines of, 224 
imperfect, where frequently en- 
countered, 258 
interprismatic substance of, sus- 
ceptibility to acids, 219 
malacotic, mass density of, 226 
native, mass density of, 226 
normal, description of, 217 

microscopic appearance of, 217 
pearl, 286 

of primitive races, 225 
organ, functions of layers of. 246 
layers of, 24 4 

of seeond permanent molar, 245 
time of appearance, for decidu- 
ous teeth, 2 \'< 
origin of word, 22:; 
porosity of, 226 

perfection in development of, 217 
permeability, degrees of, 226 
pit form defect of, 263 
reddish brown discoloration of, 259 
ridges and furrows in. 223 
rods, description of, 219 

imperfect calcification of, 253 
insufficient formation of, 260 
on axial surfaces. - 
under high magnification, 220 
washing away of, 332 
sclerotic, mass density of, 22(3 
surface, not smooth, 223 
temporary arrest of calcification in, 

253 
thickness, variations in, 218 
unvarying hardness of, 228 
white spot in, 258 
Enameloblasts, 245 

Endocarditis from oral foci of infec- 
tion, 553 
Endothelia, 36 
Endotheliomata. 146 
Endotoxins, 153 



582 



INDEX 



Entameba histolytica, 185 
Enterorrhagia, 85 
Entoderm, 35 

tissues derived from, 36 
Eosinophiles, 99 
Epistaxis, 85 
Epithelial band, 24 

cells in pulp hypertrophy, 531 

cord, 241 

invagination of, 244 

debris, 407 

remnants in peridental membrane, 
527 
Epithelioma, 141 
Epithelium of gingiva?, functions of, 

379 
Equinia, 171 

Erosion by sodium acid phosphate, 
360 

duplication in laboratory, 359 

etiology of, 359 

from lactic acid, 360 

pathologic anatomy of, 365 
Erysipelas, 156 
Erythrodextrin, 322 
Etiology, definition of, 213 

of abrasion, 356 

of caries, 322 

of diseases, 37 

of emboli, 93 

of enamel caries, 331 

of erosion, 359 

of geminated teeth, 284 

of septic apical pericementitis, 415 
Eustrongyles gigas, 206 
Extractions, tooth movement follow- 
ing, 379 
Exudate, inflammatory, 99 

inflammatory serous, 435 
Exudation, 95 

Eye involvement from impacted third 
molars, 297 



Face, involvement of, in dentoalveolar 

abscess, 429 
Facial pain from impacted third 

molars, 297 
False membranes, 74 
Fatty degeneration, 48 
Fatty infiltration, 59 
Favu's, 183 
Fermentation, lactic acid from, 315 

of carbohydrates, degrees of, 323 

of glucose, 323 

of lactose, 323 



Fertilization, 34 
Fetor of breath, 389 
Fever, agstive-autumnal, 189 
quartan, 189 
relapsing, 179 
Eocky Mountain, 195 
tertian, 189 
Texas cattle, 189 
typhus, 194 
yellow, 193 
Fibers, encased in cementum, 234 
Fibrillae, dentinal, 228 
Fibrin ferment, 74 
Fibroadenoma, 139 
Fibroblasts, 99, 108, 406 

of repair, 443 
Fibroids, recurrent, 127 
Fibroma, uterine, 131 
Fibromata, 117 

soft, 118 
Filariasis, 205 
Fissures, caries in, 334 

defective, calcified amorphous bodies 

in, 260 
defective, in molars and bicuspids, 

318 
perfect, in molars and bicuspids, 318 
Flatworms, 195 
Focal necrosis, 78 
Foci of infection, 544 
chronic, 422 
endocarditis from, 553 
extraosseous, 549 
intraosseous, 549 
most common, 551 
oral, arthritis from, 553 
secondary, 562 
Follicular cysts, 534 

pathologic, anatomy of, 540 
sac, 247 
wall, 233 

functions of, 248 
Foot and mouth disease, 194 
Formaldehyde, irritation by, 408 
Fractures, intraalveolar, of roots, 419 
Frostbite, 42 
Functions of gingiva?, 378 

of peridental membrane, 402 
Fungus nematodes, 145 
Furuncle, 103 



G 



Gallstones, 70 
Gangrene, 79 
dry, 79 
moist, 79 
of pulp, 523 
primary, 79 



INDEX 



583 



Gangrene — Cont 'cl. 
secondary, 79 
senile, 80 
Gaseous edema, 177 
Gelatinous plaques, 331 
Germicidal concentrations, effects of, 

409 
Germicides, mild, in root infections, 

410 
Geminated, deciduous teeth, 284 
Geminated teeth, 284 
Germ plasm, 40 
Giant cells, of repair, 107 
Gingiva, relation to peridental mem- 
brane, 403 
Gingiva?, body of, 376 

chronic inflammation of, photomi- 
crograph of, 395 
classification of, 376 
free, 377 

functions of, 378 
internal aspect of, 379 
normal and pathologic considera- 
tions, 376 
peridental membrane fibers in, 377 
septal, 377 
of sheep, 376 
Gingival epithelium, functions of, 379 

irritation, 391 
Gingivitis by salivary deposits, 389 
chronic, 392 

advanced, p h o t o m i c rograph 

stage, 396 
progressive photomicrograph of, 

398 
pathologic anatomy of, 392 
involvement of peridental mem- 
brane fibers in, 393 
Glanders, 171 
Gleet, 157 
Glioma, 132 

ganglionic, 133 
Globulins, 28 

Glucose, fermentation of, 323 
Glycogenic infiltration, 71 
Glycoproteins, 28 

Glycosuria, artificially induced, man- 
ifestations in saliva, 374 
Gonorrhea, 157 
Gouty diathesis, increase of chlorides 

in, 372 
Granular degeneration, 48 
Granular layer of Tomes, 231 

relation of to dental caries, 326 
Granulation tissue in pulp hypertro- 
phy, 530 
Granuloma, dental, 423, 355, 436, 549 
objections to term, 438 



Granulomata, infectious, 164, 438 

Growth, giant, 111 

Guinea worm disease, 205 

Gum recession, attempts to remedy, 

388 
Gumma, 170 
Gums and gingivae, 375 

blood supply of, 375 

histology of, 375 



II 



Habits, as a predisposing cause, 40 

Haplobacteria, 153 

Hard and soft teeth, 226 

Harelip, 211 

Healing by first intention, 106 

by second intention, 106 

by third intention, 107 
Health, definition of, 21 
Heat, exciting cause of disease, 41 

exhaustion, 42 
Helmintlies, 195 
Helminthiasis, 195 

Hematogenic route, periapical infec- 
tion by, 421 
Hemangiomata, 134 
Hematidrosis, 85 
Hematocele, 85 

Hematogenous pigmentation, 63 
Hematoidin, 66 
Hematoma, 86 
Hematemesis, 85 
Hematuria, 85 
Hemoglobin, 29, 66 
Hemopericardium, 85 
Hemopeiitoneum, 85 
Hemophilia, 87 
Hemoptysis, 85 
Hemorrhage, 85 
Hemorrhagic infarct, 86 
Hemorrhage, secondary, 86 
Hemosiderin, 64, 66 
Hemothorax, 85 
Hepatization, 160 
Hepatogenous pigmentation, 63 
Heredity and absence of teeth, 291 

and caries, 321 

and disease, 40 
Herpes labialis, 572 
Heterolysis, 76 
Heteroplasia, 110 
Histologic defects in enamel, 253 
Histology, morbid, definition of, 213 

of gums and gingiva?, 375 

pathologic, 37 
HoAvship's lacunae, 470 



584 



INDEX 



Hutchinson's notch, 266 

teeth, 269, 299 

triad, 304 
Hyaline degeneration, 54 
Hyaloplasm, 25 
Hydrocephalus, 96 
Hydropericardium, 96 
Hydroperitoneum, 96 
Hydropic infiltration, 71 
Hydrops, articuli, 96 
Hydrorrhachis, 96 
Hydrothorax, 96 
Hylomata, 116 

Hyperacid diathesis, ammonium car- 
bonate in, 372 
Hypercementosis, 350 

and pulp removal, 355 

and pyorrhea alveolaris, 355 

causes of, 353 

etiology and pathologic anatomy, 
352 

from mild infection, 354 

from occlusion stress, 353 

from protruding root filling, 354 

from rough edges of fillings, 353 
salivary an 
posits, 353 

from thread biting, 353 

from tooth movement, 353 

in chronic dentoalvcolar abscess, 
354 

in lower molars, 351 

in upper bicuspids, 351 

in upper molars, 351 
Hyperemia, 83 

active, 83 

collateral, 83 

neuroparalytic, 83 

neurotic, 83 

of pulp, 505, 518 

passive, 84 
Hypernephroma, 148 
Hyperostoses, 121 
Hyperplasia, 111 
Hypertrophy, 111 

'false, 11 i 

numerical, 111 

of pulp, 530 

simple, 111 

true, 111 
Hyphomycetes, 152 
Hypoplasia, 45, 250 

of cervico-lingual ridge, 265 

dental, causes of, 252 
microscopic, 251 
milder forms of, 260 
pathologic anatomy of, 258 

of deciduous teeth, 258 



Hypoplasia — Cont 'd. 

of dentin, 256 

of enamel and caries, 317 

of enamel producing external de- 
fect, 255 

of lower first bicuspid, 277 

of lower cuspid, 270 

of lower second bicuspid, 277 

of upper cuspid, 269 

of upper third molar, 283 
Hypoplastic enamel, predisposition to 
causes of, 318 



Idiosyncrasy, 39 

Imbrication lines and caries suscep- 
tibility, 225 
Immune, saliva of, 315 
Immunity, 153 
acquired, 153 

from dental caries on, 315 
natural, 154 
Impaction of third molars, case his- 
tories, 296 
Incisor central, abrasion of, 362 

disproportion in size of crown 

and root, 266 
imperfect development of root, 

266 
macroscopic deformities of, 264 
overdeveloped, 266 
supernumerary root in, 265 
with short root, 267 
lower lateral, abnormalities of, 269 
lower central, freedom of defects 

of, 267 
upper lateral, abnormalities of, 267 
absence of, 291 
deflection of root of, 268 
peg-shaped, 268 
Incisors, abrasion in, 358 

supernumerary tuberculated, 287 
[incremental lines, 221 
Indol, 524 

Infantile paralysis, 192 
Infantilism, 45 
Infarcts, 92 

anemic or white, 92 
hemorrhagic, 86 
hemorrhagic or red, 93 
Infection, 152 
infectious protozoa, 185 
infestation, 152 

Inhibition, pain a source of, 294 
Infiltration, :>9 
calcareous, 68 
fatty, 59 



INDEX 



585 



Infiltration— Cont 'cl. 

glycogenic, 71 

hydropic, 70 

interstitial, of fluid, 95 

pigmentary, 61 

round-cell, 99 

serous, 70 / 

Inflammation, 98 

acute, 98 

acute, characteristics of, 99 

catarrhal, 104 

chronic, 98 

chronicity and acuteness of, 424 

diphtheritic, 100 

edematous or serous, 100 

fibrinous, 100 

follicular, 105 

hemorrhagic, 106 

interstitial, 106 

of gingiva and gums and dental 
caries, 320 

parenchymatous, 105 

phlegmonous, 103 

phlegmonous, of face, 431 

productive, 106 

septic, of peridental membrane, 412 

suppurative, 101 
Inflammatory exudate, 99, 435 
Influenza, 178 
Interglobular spaces, 231 

abnormal in size and number, 256 
abundance of, 319 
Interprismatic substance, dissolution 
of, 325 
susceptibility to acids, 219 
Interproximal spaces, flat, 319 
Ionization, 30 
Irritability, 32 
Irritation by formaldehyde, 408 

gingival. 391 
Ischemia, 82 



Jaws, necrosis, bacterial causes of, 
464 
chemical causes of, 464 
diagnosis of, 463 
mechanical causes of, 463 
osteitis of, 470 
osteomyelitis of, 469 
periostitis of, 467 
rarefying osteitis of, 462 



K 



Karyoplasm, 25 

Karvosomes, 26 
Keloids, 117 



Lactic acid, end product of fermenta- 
tion, 315 
in depth of dentin, 328 
in erosin, 360 
Lactose, fermentation of, 323 
Lacunge of cementum, 233, 235 
Lamellae of cementum, 233 
Leishmaniases, 187 
Lepedomata, 116 
Leptothrix infections, 180 
Leprosy, 167 
Leptus autumnalis, 206 
Leucin, 524 

Leucocytes in chronic dentoalveolar 
abscess, 444 
mononuclear, 448 
polymorphonuclear, 99 
eosinophile, 447 
neutrophile, 444 
Leueoplakia of tongue, 573 
Leukoderma, 67 
Life, simpler forms of, 26 
Lime salts, extraction of, from teeth, 

316 
Linin, 26 
Lipoids, 29 
Lipomata, 122 
Liquefaction necrosis, 75 
Lock jaw, 172 
Lues, 168 
Lumpy jaw, 181 
Lung dust disease, 61 
Lymphangiomata, 135 
Lymphatic vessels, obstruction of, 95 
Lymphocytes, 99, 447 
Lymphosarcoma, 125 
Lysins, 153, 76 

M 

Macroscopic pathology, 37 

Madura foot, 182 

Malacotie enamel, mass density of, 

226 
Malaria, 187 

Plasmodium of, 187 
Malarial pigmentation, 62, 63 
Malformations, 208 

by defect, 208, 209 

by excess, 208 

by perversion, 208, 211 

due to defective development in 
anterior median line, 209 

due to defective development in 
posterior median line, 209 
Malignant edema, 177 
Malocclusion and abrasion, 356 

and dental caries, 319 



586 



INDEX 



Maltose from starch, 

Maori race, caries in, 313 

Malta fever, 176 

Maltase enzyme, 323 

Maltose, hydrolysis of, 323 

Mummification, 79 

Mandible, sinuses on lingual aspect, 

429 
Marrow, 456 
red, 456 
yellow, 456 
Matrix of cementum, 234 
Maxillary sinus, abscess discharging 
into, 427 
infection from cell, 427 
variations in shape and size, 427 
Measles, 190 
black, 190 
German, 191 
Meat diet and dental caries, 320 
Meat-eating tribes and caries, 312 
Medullary substance, 458 
Melanocarcinoma, 146 
Membranes, false, 74 
Meningitis, epidemic cerebrospinal, 

156 
Menorrhagia, 85 
Mercurial stomatitis, 569 
Mesoderm, 35 

tissues derived from, 36 
Metabolic pigmentation, 62 
Metaplasia, 110 
Metaplasm, 25 
Metastasis, 92 
Metazoa, 152, 195 
Metrorrhagia, 85 
Micrococcus gonorrheae, 157 

tetragenus, 155 
Microorganisms, pathogenic for man, 

152 
Microscopic pathology, 37 
Mites, 196 

Molars and bicuspids, discoloration 
on approximal surfaces, 334 
defective fissures in, 318 
first permanent, disturbances affect- 
ing development of, 253 
noneruption of, 293 
fourth, 289, 290 

impacted third, and disturbed pho- 
nation, 298 
ear involvement from, 297 
eve involvement from, 297 
facial pain from, 297 
lower first, disto-buccal cusp, ab- 
sence of, 281 



supernumerary root in, 



Molar 

lower first, 
281 

lower, hypercementosis in, 351 
lower second, abnormalities of, 282 
lower second, with four roots, 282 
lower third, dwarfed, 282 
lower third, supernumerary root of, 

283 
second, impaction of, 297 
second permanent, origin of enamel 

organ of, 245 
third permanent, origin of enamel 

organ of, 245 
perfect fissures in, 318 
supernumerary, 289 
third, upper and lower, abnormali- 
ties of, 283 
impacted, 294 

case histories, 296 
reflexes from, 294 

reflex disturbances from, 296 
upper first, fusion of roots of, 280 
supernumerary cusp in, 280 
hypercementosis in, 351 
second, abnormalities of, 281 
third, dwarfed, 282 
hypoplasia of, 283 
supernumerary root in, 284 
Molds, 152 
Mole pigmented, 135 
Molluscum contagiosum, 142 
Mononuclear wandering cells, origin 

of, 449 
Monosaccharides, 324 
Morbid anatomy, 37 
Morula, 34 
Motility, 32 

Mouth bacteria, number of, 315 
infection and cancer, 561 
and systemic disease, 544 
and tuberculosis, 561 
as a source of systemic intoxica- 
tions, 555 
dry, and dental caries, 316 
washes, weak acids in, 332 
Mucin, 28, 369 

in plaque formation, 331 
precipitation of, 370 
Mucoid degeneration, 50 
Mucous membrane of gingivae and 
gums, 375 
of hard palate, 375 
patch, 136 
Mumps, 191 
Mycetoma, 182 
Mycoses, 152, 180 
Myxomata, 119 



INDEX 



587 



N 

NaCl, increased, 95 

Nanism, 45 

Nasal cavity, abscess discharging into, 

427 
Nasmyth's membrane, 246 
Necrobiosis, 72 
Necrosis, 72 

coagulation, 73 

fat, 77 

focal, 78 

liquefaction, 41, 75 

cheesy, 76 

of alveoli, 462 

of jaws, bacterial causes of, 464 
causes of, 463 
chemical causes of, 464 
diagnosis of, 463 
mechanical causes of, 463 
Nematodes, 196 
Neoplasm of pulp, 508 
Nevus, 135 
Neuridin, 413, 524 
Neurin, 413 

Newman, sheaths of, 230 
Nitrogenous decomposition, 413 
Nodules, pulp, 514 
Nonelectrolytes, 30 
Nucleolus, 26 
Nucleoplasm, 26 
Nucleus, 25 







Occlusion stress, hypercementosis 

from, 353 
Occupations, injurious, 40 
Odontoblastic layer, 230 
Odontoblasts, 247, 500 
Odontomas, cystic, 532 
Oidiomycosis, 183 
Opsonins, 153 

Ophthalmia neonatorum, 157 
Oral disease, definition of, 213 
Oral foci of infection, 544 
Organic disease, 216 

matter, comparison in cementum 
and bone, 240 
Osmosis, disturbed, 95 
Osteitis, of jaws, 470 

rarefying, 462 
Osteoblasts, 407 
Osteoclasts, 407, 456 
Osteogenetic layer of periosteum, 456 
Osteomalacia of pregnancy, causes of, 
320 



Osteomata, 121 

heteroplastic, 121 

homoplastic, 121 
Osteomyelitis, 394 

acute, in dentoalveolar abscess, 435, 
457, 469 
Osteophytes, 121, 467 
Oxuris vermicularis, 202 
Oxygen tension, change of, in root 
canal, 414 



Pain, continued, action of, 294 
Palate, hard, mucous membrane of, 

375 
Papilla, dental, 246 
Papillomata, 135 
hard, 136 
intracystic, 136 
soft, 136 
Paralysis, infantile, 192 
Paraplasm, 25 
Parasites, 152 

facultative, 152 
Parenchymatous degeneration, 48 
Parotitis, acute epidemic, 191 
Parules, 431 
Pasommoma, 147 
Pathologic anatomy, 37 
definition of, 213 
of chronic gingivitis, 392 
chemistry, 37 
Pathology, cellular, 123 
dental," definition, 213 
general, definition, 21 
general and dental conception of, 

216 
gross, 37, 216 
Pathologic histology, 37 
physiology, 216 
processes, 45 
Pediculus capitis, 196 
pubis, 196 
vestimenti, 196 
Petechia?, 86 
Peptides, 27 
Peptones, 27 

Perforations of root canals, 419 
Periapical infection by hematogenic 

route, 421 
Periapical infections, recovery from, 

422 
Pericemental abscess, 422 
of gouty origin, 496 
inflammation, acute septic, 412 
septic, 412 
septic, summary of causes, 421 



588 



INDEX 



Pericementitis, acute septic, 412 
chronic septic, 412 
first symptoms of, 433 
nonseptic, 408 
nonseptic, caused by protruded root 

fillings, 410 ' 
nonseptic, causes of, 408 
nonseptic, from arsenic, 410 
nonseptic from pressure, 410 
nonseptic, from pulp extirpation, 

410 
septic apical, 422 
bacteria of, 452 
etiology of, 45 
Pericementum, 402 
Peridental membrane, 248 
apical fibers, 406 
atrophy of, 491 
blood supply of, 402, 407 
cysts from chronic infection of, 

441 
diseases of, 402 

effect of mild irritation upon, 352 
epithelial remnants in, 442, 527 
fibers of, 404 

fibers, detachment of, 439 
free gingiva fibers, 406 
functions of, 402 
horizontal fibers of, 405 
involvement in gingivitis, 393 
nerve supply of, 407 
oblique fibers of, 405 
relation of, to gingiva, 403 
septic inflammation of, 412 
structural constituents of, 406 
susceptibility to infectious proc 

esses, 402 
transseptal fibers, 406 
thrombi in, 410 
Periosteum, 456 

Periostitis, acute, in dentoalveolar ab- 
scess, 431, 435 
Pernio, 42 
Pertussis, 179 

Periostitis, chronic, osteophytes in, 
467 
of jaws, acute, 467 
symptoms of, 469 
syphilitic, 470 
Phleboliths, 381 
Phonation, disturbed, from impacted 

third molar, 298 
Phosphoproteins, 29 
Physiochemical processes in tissues, 

21 
Physiology, pathologic, definition of, 

213 
Pickerills' calcarine fissures, 225 



Pigment, malarial, 63 
Pigmentary infiltration, 61 
Pigmentation, hematogenous, 63 

hepatogenous, 63 

malarial, 62 

metabolic, 62 

of dentin in caries, 347 
Pigments, metabolic, 63 
Pits, caries in, 334 
Plague, bubonic, 177 
Plaque formation, mucin in, 331 
Plaques, gelatinous, 331 
Plasma cells, 99, 451 
Plasmodium malaria?, 187 
Plastids, 25 
Platyhelminthes, 195 
Pneumonia, 159 

aspiration, 163 

fibroid, 163 

hypostatic, 163 

lobar or croupous, 159 

lobular, 161 

purulent, 163 

tuberculous, 164 
Pneumonokoniosis, 61 
Pocket formation, bone lesion in, 39 I 
Poisons, chemical, 44 
Poliomyelitis, acute, 192 
Polyarthritis, 193 
Polymorphonuclear leucocytes, 445 
Polysaccharides, 325 
Poulticing, results of, 428 
Predisposing causes, 213 
of dental caries, 320 
Pregnancy and dental caries, 320 
Pressure, effect of, 41 
Processes, retrograde, 45 
Protamines, 28 
Proteins, 27 

conjugated, 28 

simple, 28 
Proteoses, 27 
Prothrombin, 74 
Protoplasm, 23 
Protoplasmic movement, 32 
Protozoa, 23, 152 

classification of, 185 
Psoudomelanin, 63 
Pseudomucin, 52 
Ptyalin, 370 

role in caries, 370 
Pulex cheopis, 196 

irritans, 196 

lipines, 196 

penetrans, 196 



INDEX 



589 



Pulp abscess, 530 

areas of chronic inflammation in, 

507 
blood vessels of, 504 
calcific degenerations of, 510 
cells of, 503 
description of, 500 
clinical aspect of diseases of, 505 
congestion, 521 
constructive changes in, 506 
death, chemical causes of, 523 
death, mechanical causes of, 523 
death of, en masse, 523 
decomposed, 413 
degenerations, 508 
degeneration in abrasion, 358 
diseases of, 505, 500 

exciting causes, general, 508 

exciting causes of (local), 509 

local predisposing causes of, 507 

predisposing causes of, 506 
exposure in abrasion, 357 
gangrene, 523 

gangrenous, organisms in, 452 
histologic constituents of, 500 
hyperemia. 505, 518 

active, 518 

character of pain from, 522 

etiology of, 520 

following insertion of gold fill: 
ings, 521 

from erosion and abrasion, 521 

in febrile disturbances, 508 

passive, 518 
hypertrophy, calcareous formations 
in', 530 

epithelial cells in, 531 
impairment of vitality, 505 
infection in absence of caries, 527 

ulcerative form, 530 
intercellular substance of, 504 
involvements, prophylaxis of, 414 
lead-wire formation in, 517 
live, abscess in teeth with, 422 
moist gangrene, 524 
mummification, 523 
neoplasm, 508 
nerves of, 504 
nodules, 514 

from erosion and abrasion, 517 
normal, 501 
Pulp, odontoblastic layer of, 230 
putrefaction, 413 

discoloration from, 524 

products of, 524 
putrefactive changes in, 525 
putrescent, 523 

organisms in, 524 



Pulp— Cont 'd. 

removal and hypercementosis, 355 
reparative power of, 529 
retrograde changes in, 506 
severe inflammation of, 425 
suppurating, organisms in, 452 
suppuration, 413, 528 
temperature, range of, 520 
thrombosis in, 523 
Pulpitis, 525 

chronic hypertrophic, 530 
nonseptic, 525 

pathologic anatomy of, 528 
septic, 526 

character of pain in, 527 
Pus, 101 
Pus pocket, 394 
Pustule, 103 
Putrefaction of pulp, 413 

products of. 524 
Putrefactive changes in dentinal tu- 
buli, 414 
changes in, pnlps, 525 
Putrescin, 413. 524 
Pyemia, 103, 154 
Pyogenic bacteria in apical region, 

412 
Pyorrhea alveolaria and hypercemen- 
tosis. 355 
and malposition of/teeth, 379 
bacteria in. 551 / 
bacteriology of. 491 
by salivary calculi, 474 
by subgingival deposits, 476 
clinical forms, 473 
defective approximal contacts in, 

479 
food impactions in. 47^ 
general considerations. 47°, 
historical sketch, 471 
indicative of, 473 
of gouty origin, 495 
of systemic origin, 487 
osteomyelitis in, 484 
substitute terms for, 473 
systemic disorders and, 485 
systemic factor in, 490 
systemic lesions by bacteria 
from, 551 
pockets, study of culture of, 494 



E 



Race as a predisposing cause, 39 
Earefaction areas, 419, 554 
Barefving osteitis. 462 

of alveoli, 462 

of jaws, 462 



590 



INDEX 



Baynaud's disease, 82 

Beflexes from impacted third molars, 

294 
Eegeneration, 108 
pathologic, 108 
physiologic, 108 
Eenal calculi, 70 
Eelapsing fever, 179 
Beproduction, 33 
Eesorption of apical areas, 465 

of cementum, 250 
Eetrograde processes, 45 
Eetzius, bands of, 221 
in hypoplasia, 262 
Bidge, cervicolingual fissured, 265 
Bhabdomyoma, 130 
Eheumatism, acute articular, 192 
Bhinoscleroma, 171 
Khinoliths, 70 
Biggs' disease, 473 
Bingworm, 183 
Bocky Mountain fever, 195 
Eodent ulcer, 142 
abrasion of, 357 

bifurcation in upper second bicus- 
pid, 273 
cysts, 532 

deflection in upper first bicuspid, 
271 
Boot 

canals, irritating drugs in, 408 

perforation of, 419 
of central incisor, imperfect de- 
velopment of, 266 
filling beyond apical foramen, ef- 
fects of, 353 
fractures, intraalveolar, 419 
fusion of, in upper first molar, 280 
of upper second bicuspid, abnor- 
malities of, 271 
perforation, 411 

supernumerary, in central incisor, 
265 
in lower cuspid, 273 
in lower first molar, 281 
in lower third molar, 283 
in upper third molar, 284 
two, in lower bicuspids, 277 
in lower cuspid, 270 
in lower cuspids, 272 
in lower lateral incisor, 269 
in upper second bicuspid, 274 
Eubeola, 190 



S 



Saeeharomyces albicans, 571 
Saliva, 366 

abnormal constituents of, 373 



Saliva — Cont 'd. 

action on blood cells, 315 

albumin in, 371 

amount of, 366 

color of, in pathologic and normal 

states, 367 
hemolytic power of, 315 
immunizing properties of, 315 
immunizing properties of, and den- 
tal caries, 315 
inorganic constituents of, 369, 372 
manifestation in, of excessive car- 
bohydrate intake, 374 
odor of, in pathologic and normal 

states, 368 
of immunes, 315 
of immunes to caries, 315 
of susceptibles to caries, 316 
on antiseptic power of, 315 
organic constituents of, 369 
parotid, unmixed, 383 
quantity of, in relation to caries, 

316 
reaction of, 373 
solution of blood cells by, 315 
sulphocyanat.es in, 371, 372 
taste of, in normal and pathologic 

states, 368 
viscosity of, 316 

in relation to caries, 316 
Salivary calculus, agglutinin of, 384 
destruction of investing tissues 
by, 388 
Salivary 

deposits and hypercementosis, 353 
as cause of gingivitis, 389 
clinical symptoms of, 389 
color of, 386 

denudation of cementum by, 388 
effects of, 389 
from betel-nut chewing, 383 
in salivary glands, 381 
lesions caused by, 387 
location of, 381 
origin of, 381 
size of, 386 

theories on formation of, 381 
where first formed, 388 
depressants, 366 
depressants of potential acidity, 

312 
glands, deposits in, 381 
stimulants, 366 

in relation to caries, 312 
Sapremia, 154 
Saprophytes, 152 



INDEX 



591 



Saprophytic bacteria, action of, 113 

organisms in acute dentoalveolar 
abscess, 433 
Sarcoma, alveolar, 125 

giant-celled, 128 

melanotic, 127 

round cell, 121 

spindle-celled, 127 
Sarcomatous cvlindromata, 126 
Scarlatina, 191 
Scarlet fever, 191 
Scalorrhea, 367 
Schizomycetes, 152 
Sclerometer, enamel, 228 
Sclerotic enamel, mass density of. 226 
Secondary dentin, 511 
' ' Self -cleaning, ' ' as applied to teeth, I 

319 
Septal gingivae, 377 
Septal tissues and caries, 337 
Septic pericemental inflammation, | 

acute, 112 
Septicemia, 151 
Sequestrum formation in chronic 

dentoalveolar abscess, 468 
Serous infiltration, 71 
Serum, antidiphtheritic, 173 

antitetanic. 172 
Sharpey 's fibers, 456 
Sheaths of Newman, 230 
Shock, 11 

Shreger, lines of, 222 
Sialorrhea, 367 
silicosis, 61 
Sinus formation. 127 
Sleeping sickness, 186 
Smallpox, 191 
Sodium phosphate, acid, in erosion, 

360 
Solution, 30 
Somatic death, 73 
Specific gravity of enamel, compared 

with density, 226 
Sphacelous. 73 

Spirillum cholera Asiaticae, 173 
Spirocheta pallida, 108. 305 
Spirochetae obermeieri, 179 
Spongioplasm, 25 
Sporotrichosis. 181 
Sporothrix, 181 
Stain, lirown. of enamel, 259 
Staphylococcus epidermidis albus, 155 

pyogenes albus. 155 

pyogenes aureus, 155 
Starch, 325 

conversion of, into maltose, 322 
Starchy foods and dental caries, 320 
Stellate reticulum, 211 



Stomatitis aphthous, 570 

pathologic anatomy of, 570 
catarrhal, 566 

pathologic anatomy of, 567 
mercurial, 569 
simple, 565 

pathologic anatomy of, 566 
simplex, 565 
ulcerative, 567 

pathologic anatomy. 567 
Stratum intermedium, 211 
Streptococci, in chronic dentoalveolar 

abscess. 152 
Streptococcus erysipelatis, 156 
mucosus, 152 
pyogenes, 155 
rheumaticus. 156 
viridans, 156, 152. 551, 552 
Stricture, 157 

Strongyloides intestinalis, 202 
Subgingival deposits, 390 

ami hypercementosis, 353 
color of, 390 
detection of, 392 
etiology of, 390 
lesions produced by. 392 
preliminary step in formation, 
396 
space, bacterial absorption from, 
380 
penetration of bacteria through, 
122 
Submental fistula, 130. 131 
Sugars, double. 321 

multiple, 325 
Sugars, relative fermentability of, 323 

simple, 321 
Sulphocyanates, amount of. in saliva, 

* 372 
" ' Sulphur granules, ' ' 181 
Sunburn, 13 

Sunlight, bactericidal action of, 13 
Sunstroke, 12 

Supernumerary cusp in upper first 
molar, 280 
molar, 289, 290 
peg-shaped tooth, 287 
root in central incisor, 265 
root in lower first molar, 281 
root in upper third molar, 281 
tuberculated incisors, 287 
teeth. 2^7 
Suppurative inflammation, 101 
Suppuration, description of, 113 

in pulp. 113 
Swelling from dentoalveolar abscess, 
^ 131 



592 



INDEX 



Syphilis, 168 

dental manifestations of, transmis- 
sion to fetus, 253 

hereditary, dental stigmata of, 303 

pathognomonic signs of, 303 

primary stage, 169 

secondary stage, 169 

tertiary stage, 169 

transmission of, 299 
Syphilitic stigmata, 299 
Syringomyelia, 96 



T 



Tapeworms, 195, 198 
Teeth, abnormalities of, 250 

abraded, discoloration of dentin in, 

347 
absence of, 291 
calcium salt content of, 226 
classification of, as to hardness, 226 
deciduous, calcification of, 248 
geminated, 284 
hyperplasia of, 258 
retention of, 291 
time of appearance of enamel or- 
gans for, 245 
development of, 241 
extraction of lime salts from, 316 
fully calcified, noneruption of, 294 
geminated, 284 
Hutchinson's, 299 
macroscopic deformities of, 264 
malposition in pyorrhea alveolaris, 

379 
mass density of, 227 
permanent, calcification of, 248 
• • self-cleansing, " 319 
specific gravity ami density, differ- 
ence between, 226 
supernumerary, 287 
Tenderness to pressure in pericemen- 
tal infection, 425 
Teratomata, 148 
Tetanus, 172 
Thrombi, 74 

agglutinative, 88 

annular, 88 

arterial, 88 

ball, 88 

calcified, 89 

canalized, 89 

capillary, 88 

cardiac, 88 

eonglntinative, 88 

hyaline, 88 

infective, 89 

in peridental membrane, 410 



Thrombi— Cont 'd. 

lymphatic, 88 

marantic, 88 

obliterative, 88 

organized, 89 

parietal, 88 

polvpoid, 88 

portal, 88 

primary, 88 

propagated (secondary), 88 

proximal, 88 

red, 88 

saddle, 88 

stratified, 88 

types of, 87 

valvular, 88 

venous, 88 

white, 88 

yellow, 88 
Thrombosis, 87 
Thrush, 571 

pathologic anatomy of, 572 
Ticks, 196 
Tinea, circinata, 184 

favosa, 183 

sycosis, 184 

tonsorans, 184 

triehophytina, 183 

versicolor, 184 
Tissue changes, progressive, 111 
Tissues, investing, destruction of, by 
salivary calculi tobacosis, 61 
Tomes, filters of, 505 

granular layer of, 231 

zone of 344 

zone of, possible etiology of, 346 
Tongue, affections of, 572 

leucoplakia of, 573 

ulcers of, 572 
Tooth brush friction and abrasion, 
356 

development, first evidence of, 242 

follicle, fibrous envelope of, 233 

impaction, 291 

Incarceration, 291 

movement, following extraction, .".79 

peg-shaped, supernumerary, 287 

powders, gritty, and abrasion, 356 

protrusion, 426, 433 

sensory organ of, 500 
Toxemia, 154 

Toxic products from burned tissue, 42 
Toxins, 153 

intracellular, 153 

soluble, 153 
Transparent zone, 344, 510 
Transudation, 95 
Traumatisms, 39 



INDEX 



593 



Trematodes, 195, 196 
Treponema pallidum, 168 
Trichinosis, 204 
Trichoeephalus dispar, 202 
Trichomycetes, 180 
Trichophyton, 183 
Trypanosomes, pathogenic, 186 
Trypanosomiasis, 186 
Tuberculosis, 164 

and mouth infection, 561 
secondary, 167 
Tubular calcification in abrasion, 35! 
Tubuli, dentinal, 228 
a field of, 229 
anastomosis of, 230 
average diameter of, 348 
calcific degeneration of, 510 
curves of, 231 

in bicuspids and molars, 230 
in incisal region, 230 
in relation to cusps, 231 
penetration into enamel, 232 
relative diameters of, 230 
Tumors, 113 
benign, 115 
classification of, 116 
habit of growth theory, 114 
inclusion theory, 113 
irritation theory, 113 
nervous theory, 114 
parasitic theory, 114 
predisposing causes, 114 
primary, 115 
secondary, 115 
theories of origin, 113 
Typhoid fever, 174 
Typhus fever, 194 
Ty rosin, 524 

U 
Ulcer, 104 

follicular, 104 
fungous, 104 
gangrenous, 104 
indolent, 104 



Ulcer — Cont 'd. 

of tongue, 572 

peptic, 104 

phagedenic, 104 

rodent, 142 

serpiginous, 104 

specific, 104 
Ulceration form of infection of pulp, 

530 
Uric acid salts in blood, 496 



V 



Vaccination, 154 
Varicella, 191 
Variola, 194 
Venucse, 136 
Vesical calculi, 70 
Vincent's angina, 179 
Viscosity of saliva, 316 
Vital resistance, 214 

conditions which lower, 214 

lowered, 214 
Volkmann 's canals, 455 

W 

Wandering cells, 99 
Warts, 136 
Wheals, !'.', 
" White 7 ' clots, 75 
Wombstones, 132 
Worms, round, 196 



Xanthoma, 128 



Veasts, 152 



Zone of Tomes, 344 






sfi 






\\ 



